What I did before

Chronic pain is under-recognized and under-treated.  It affects people of all ages, races and socioeconomic class and there are many different types of chronic pain. In Canada, one in five people suffer daily from chronic pain. Our patients with chronic pain have unique and complex needs often needing longer office visits. It can be very challenging to help patients to navigate the health care system. As a family physician it was difficult to discuss issues in a systematic, integrated and holistic way within a short office visit. Given our heavy patient loads and current billing paradigms, family physicians are challenged to meet the educational needs of chronic pain patients as pain education and self-management training takes a lot of time.

What changed my practice

Two websites have changed my practice.

1) The www.PainBC.ca website has changed my practice because it provides options beyond medications. It is a one stop website with BC resources, ideas and methods to help support patients outside of our office. By downloading  the pain toolbox from the website  I feel I’m better able to engage and support my patients in the management of their chronic pain.  Some suggested goals of referring patients to this resource include:

1. Engaging people living with pain in a self-management paradigm that allows them to begin learning the process of taking back their life. The website provides information on specialized health care providers, and community, government, and academic partners.
2. Providing education for people living with pain, their family friends and other health care providers
3. Facilitating our office visits to become more productive by providing referral and reference resources.

2) The People in Pain Network (PIPN) (http://www.pipain.com) hosts an online pain self-management course called the Pain Toolkit for people who can’t get to one of the face to face programs available or who have done a program but want more information. The PIPN online course can be a great resource for those who cannot attend in person support group sessions. Many patients find it helpful for ongoing help after they have completed a program either in the community or at a hospital or private pain clinic (via WBC for instance). The website also provides information on  pain support meetings and upcoming webinars and broadcasts about chronic pain.

What I do now

The key for the busy family physician is providing the information above in manageable chunks and approach care plan negotiation in partnership with our patients.

Now, with all of my patients with chronic pain, in addition to providing referrals, investigations, specialist consults, and medication changes and renewals; I can offer education and self-management resources. I negotiate with patients the agenda to discuss self-management during regular monthly follow-up appointments which is important for pharmaco-vigilance and a encouraging a systematic comprehensive approach to care.  One of my patients reminded me that it’s important to match this intervention to where they are personally in the stages of change. Patients need to be ready to change prior to introducing this concept, to even suggest some homework and book series of follow up visits.

For patients who are in the action phase of change and want to start an online pain management course, I am now recommending patients look at the PAIN TOOLKIT course at  http://bcpaintoolkit.pipain.com/.  This is a simple online guide on principles of self-management for patients with chronic pain. Another method to identify patients who would benefit from this resource is to ask some screening questions.  Dr. Squire has found the following screening questions helpful to identify patients who might benefit from being referred to the online pain tool kit course.  She often asks, “Who is on their team? How do they use pacing in their life (to manage pain)? (When managing their own chronic pain) What do they know about prioritizing and/or What relaxation skills do they use?” If patients don’t know the answer to these questions or if they agree they could use some help in one of the areas, this indicates that a review the principles of self-management that the Pain toolkit  teaches would be helpful.

The second step I am beginning to recommend or demonstrate to patients showing them how to access the PAIN TOOLBOX at Painbc which has an extensive list of topics to discuss at subsequent visits and community resources to attempt to access to support pain self-management.  The Personal Toolbox of Pain solutions, which was created by Drs. Squire, Williamson, Lau, Gromala and Pearson, has helped me change the way I think about organizing my chronic pain visits. Using the Toolbox, I instantly have a potential list of topics I can divide into manageable chunks and prioritize topics for future visits. It is important to carefully review each topic with patients during a one on one visit. If not, I’ve found simply giving your patient the website can be overwhelming and patients may not actually follow through unless the family physician leads the way.

For example, I would say, “Here is a list of important topics we could cover over subsequent visits.  Which topics do you want to prepare for and read prior to our next visit?”

1. Pain self-management and pain education courses
2. Improving sleep
3. Changing your mind and changing your pain
4. Mind body medicine for pain relief
5. Getting help-support for people with pain and disability
6. Exercise and Progressive Activity
7. Lifestyle changes

By recommending the pain toolkit as a guide to the approach to self-management in chronic pain and the pain toolbox as a resource for dealing with the issues that affect chronic pain, the busy family physician can make a visit less about prescription refills and more about building new coping skills. The visit can be made more efficient and effective by setting the ground rules early with the patient on dealing with one or two of the topics for each visit.  Moreover, inviting the patient to become part of a support group can be an important therapeutic goal of encouraging them to explore external supports. An example of what is available on the Pain BC Website is a link to the BC Chronic Pain Self Management Program . This program is a local peer taught self-management program where patients can sign up via www.coag.uvic.ca/cdsmp or 1-866-902-3767.  Finally, the PainBC website also provides lists of chronic pain multidisciplinary clinics and specialized care at painbc.ca/content/pain-clinics-and-services which can be helpful in explaining and arranging for the long term plans with patients.

In closing, for physicians managing patients with chronic pain, nothing can replace common clinical sense and it is vitally important to practice the principles of pharmacovigilance.  It is essential that we are all aware of and try to implement some of the recommendations of the Canadian Guidelines for Safe and Effective Use of Opioids for Chronic Non-Cancer Pain nationalpaincentre.mcmaster.ca/opioid which can be a guide for dealing with our patients.

Special thanks to D. Ford and B. Morrice for their assistance.

What I did before

Clostridium difficile infection (CDI) can range from asymptomatic carriage, to mild or moderate diarrhea, to fulminant and sometimes fatal pseudomembranous colitis.  Risk factors for CDI include antibiotic use, duration of hospitalization, and age >65.  In the past few years, a hypervirulent strain of C. difficile, called NAP-1, has caused hospital outbreaks that have been unusually severe and recurrent.

What changed my practice

Clinical practice guidelines, published in 2010, by the Infectious Diseases Society of America, provide treatment recommendations for initial and recurrent episodes of C. difficile. The guidelines are available free online at www.idsociety.org. They help to clarify when to use oral vancomycin versus oral metronidazole, and how to treat recurrences, which occur in 20% of patients.

What I do now

The guidelines have changed my practice in 6 ways:

1. In the hospital, when a patient has a high white blood count, I order a stool test for C. difficile. Most patients with CDI will have diarrhea, and may have abdominal discomfort or fever, but some patients will present with leucocytosis, which prompts me to consider CDI, in addition to other causes.
2. If a patient has severe CDI, I prescribe oral vancomycin 125 mg po qid x 14 days. Severe CDI is defined as a WBC>15 or creatinine >1.5x above baseline. (“Severe” can also include older patients, particularly if they are febrile or have a low albumin). For patients with mild to moderate CDI (normal WBC and creatinine), I prescribe metronidazole 500 mg po tid x 14 days. When I see patients in my office, and I’m not sure if their CDI is severe or not, I will send them for bloodwork to determine their WBC and creatinine.
3. If a patient has a recurrence of CDI after I’ve treated them, I again consider whether or not it’s severe. If it’s severe, I prescribe oral vancomycin just like I did for their initial episode. Sometimes patients who’ve initiated treatment for CDI in hospital, follow-up with their family doctor after discharge. Once the patient has completed treatment, no further investigations are required. However, if their diarrhea recurs, then they should be re-tested for C. difficile. Different labs do different types of testing for C. difficile, but all the tests detect the toxin-producing C. difficile, so you don’t have to specify which type of test you want. If patients have a second recurrence, they can receive a longer course of vancomycin as described in the guidelines. For the longer course, the vancomycin dose is tapered, then pulsed.  At this point, family physicians may decide to refer the patient to a specialist (infectious diseases or gastroenterology).
4. If a patient is very sick with CDI, and has hypotension or ileus or toxic megacolon, I ask for a surgical consult, and order a higher dose of oral vancomycin (500mg po qid) and add IV metronidazole 500 mg q8h. In very sick patients, colectomy may be necessary and can be life-saving.
5. In terms of vancomycin, I only give it orally. I never give it IV because IV doesn’t work to treat CDI.
6. Probiotics require further study, and are not recommended as standard-of-care. They may be considered as an adjunct to CDI treatment in patients with recurrent disease that is not severe, as long as there are no significant comorbidities.

One more thing for patients in British Columbia: Oral vancomycin is very expensive. Filling out a special authority form for Pharmacare allows eligible patients to qualify for coverage. These forms are available online at www.health.gov.bc.ca/exforms/pharmacare/5328fil.pdf.

Once the CDI treatment is completed, if the patient feels well, I do not re-test them for C. difficile, and I do not test their family members for asymptomatic carriage. The reason is that patients may continue to have C. difficile in their stool, but as long as it’s not causing them symptoms, treatment is not necessary.

To prevent recurrence of CDI, I tell patients to avoid antibiotics unless absolutely necessary. They should also avoid anti-secretory therapy (PPIs) if possible (see Dr. Ted Steiner’s post, thischangedmypractice.com/ppis-and-c-difficile-infection July 4, 2011).

Reference
Clinical Practice Guidelines for Clostridium difficile Infection in Adults: 2010 Update by the Society for Healthcare Epidemiology of America (SHEA) and the Infectious Diseases Society of America (IDSA). Stuart H. Cohen, Dale N. Gerding, Studart Johnson et al. Infection Control and Hospital Epidemiology, Vol. 31, No. 5 (May 2010), pp. 431-455. http://www.idsociety.org/uploadedFiles/IDSA/Guidelines-Patient_Care/PDF_Library/cdiff2010a.pdf

What I did before

Heart failure (HF) is a common condition, affecting 1% of all Canadians (1) and is associated with 4.9% of hospitalizations in Canada.(2) This results in a large burden on the health care system, with an average length of hospital stay that is nearly twice that for all other causes (12 days compared with 6.8).  Furthermore, patients with heart failure have an in-hospital mortality rate of 13.3% – triple the average rate of all other causes (4.4%).(2)

Large clinical trials have demonstrated mortality benefit for certain classes of medications in HF with reduced ejection fraction (EF).  Select beta-blockers (Carvedilol, Bisoprolol and Metoprolol SR) as well as angiotensin converting enzyme inhibitors (ACEi) and angiotensin receptor blockers (ARB) are among these agents.(3)

Prior to 2011, I used the aldosterone antagonist, spironolactone, only in patients with NYHA class III or IV (Table 1) and EF < 30% based on the results of the RALES trial.(4)

Table 1. New York Heart Association (NYHA) Classifications

What changed my practice

In January 2011, the EMPHASIS-HF (5) study was published in the New England Journal of Medicine (NEJM). The study’s aim was to determine the effects of the selective aldosterone antagonist, eplerenone, added to evidence based therapy, on the clinical outcomes of patients with systolic heart failure and mild (NYHA II) symptoms.

The study was a multicentre, international, double-blind, randomized, placebo-controlled clinical trial.  Study subjects included were patients with NYHA class II symptoms who were over 55 years old and had EF < 30% (or EF < 35% and QRS duration > 130 msec). According to the study’s inclusion criteria, these patients were already treated with ACEi, ARB (or both) as well as beta blockers at recommended/tolerated doses. Exclusion criteria included NYHA class III or IV symptoms, serum potassium greater than 5 mmol/L, and eGFR < 30 ml/min/1.73 m².

Eplerenone was initiated at the dose of 25 mg PO daily and increased to 50 mg PO daily after 4 weeks. Patients were followed up every 4 months with instructions to decrease the dose of the study drug for potassium levels 5.5-6 or stop the medication for potassium > 6.0.

The study enrolled 2737 patients and was stopped before the goal of 3100 patients recruited was achieved after an interim analysis of data revealed an overwhelming benefit in favor of using eplerenone.

Baseline characteristics were similar in both placebo and eplerenone groups with 33% of participants having a GFR of < 60 ml/min/1.73 m². Medications use at randomization included diuretics (85%), ACEi/ARB or both (94%) and beta-blocker (87%).

Results of the study showed that the primary outcome (death from cardiovascular causes or hospitalization for heart failure) occurred in 18.3% in the eplerenone group and 25.9% in the placebo group (hazard ratio (HR) 0.63; 95% CI, 0.54-0.74; p<0.001). The secondary outcome (death from any cause or hospitalization for heart failure) was met in 19.8% of patients in eplerenone group compared with 27.4% in the placebo group (HR 0.65; 95% CI, 0.55-0.76; p<0.001). In total, 12.5% of patients in the eplerenone and 15.5% of patients in the placebo group died (HR 0.76; 95% CI, 0.62-0.93; p=0.008). The numbers needed to treat to prevent one primary outcome or death per year of follow-up were19 and 51, respectively.

At the end of trial, the mean change in serum creatinine level from baseline was 8±32.7 μmol/L in the eplerenone group compared with 3.5±35.4 μmol/L in the placebo group, while potassium levels were increased from baseline by 0.16±0.56 mmol/L in the eplerenone group compared with 0.05±0.53 mmol/L (p<0.001). More patients in the eplerenone group had high potassium levels (K+>5.5, 11.8% in eplerenone group vs 7.2% in the placebo arm; K+ >6: 2.5% in eplerenone group vs. 1.9% in the placebo group, p=0.29). There were no statistically significant differences between the two groups for hypokalemia, renal failure, hypotension or gynecomastia.

What I do now

There is high mortality and morbidity associated with heart failure. Previously, aldosterone antagonists were used in patients with moderate to severe heart failure symptoms and low EF or those with reduced ejection fraction after a myocardial infarction based on RALES and EPHESUS trials, respectively (4,6).

 Based on the results of the EMPHASIS-HF study, I now use spironolactone or eplerenone in patients with EF <30-35% and NYHA class II symptoms.  Although eplerenone was studied in the EMPHASIS trial, it is thought that the clinical benefit derived is based on a class effect (7). Thus we recommend eplerenone as a first line agent in NYHA class II patients, however we believe that spironolactone can also be used if cost is a limiting factor.  Patients who develop disabling side effects from spironolactone, (gynecomastia, breast tenderness or sexual dysfunction) should use eplerenone given its specific mineralocorticoid blockade (8).

Retrospective trials have shown that while the use of aldosterone antagonists increased in the years following the publication of the RALES trial, the rates of hospitalizations for hyperkalemia also significantly increased (9). Therefore, I monitor the patients’ creatinine and potassium levels closely after initiation of an aldosterone antagonist and with each uptitration to monitor for hyperkalemia and kidney injury. Furthermore, the use of both an ACEi and ARB in combination with an aldosterone antagonist should be avoided.

Conclusion: Spironolactone or eplerenone should be added to BB and ACEi/ARB in NYHA class II HF patients with EF < 30-35% in the absence of significant renal impairment or hyperkalemia.

References (Note: Article requests might require a login ID with CPSBC or UBC):

1. Chow C-M et al. Can J Cardiol 2005;21(14):1265-71 (View article)
2. Dai S, Walsh P, Wielgosz A, et al. Comorbidities and mortality associated with hospitalized heart failure in Canada. Can J Cardiol. 2012;28(1):74-9 (View article with CPSBC or UBC)
3. Am Fam Physician. ACC and AHA Update on Chronic Heart Failure Guidelines. 2010;81(5):654-665 (View article)
4. Pitt B, Zannad F, Remme WJ, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. N Eng J Med 1999;341:709-17 (View article)
5. Zannad F, McMurray JJ, Krum H, et al. Eplerenone in patients with systolic heart failure and mild symptoms. N Engl J Med. 2011;364(1):11-2 (View article)
6. Pitt B, Remme W, Zannad F, et al. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. N Eng J Med 2003;348:1309-21 (View article)
7. Armstrong PW. Editorial. New Eng J Med. 2011;364(1):79-80Chatterjee S, Moeller C, Shah N, et al. Eplerenone is not superior to older and less expensive aldosterone antagonists. Am J Med. 2012;125(8):817-25 (View article with CPSBC or UBC)
8. Juurlink DN, Mamdani MM, Lee DS, et al. Rates of hyperkalemia after publication of the Randomized Aldactone Evaluation Study.  N Engl J Med. 2004;351(6):543-51 (View article)

What I did before

Atopic dermatitis (AD) is a chronic, itchy relapsing dermatitis that affects up to 20% of North American kids. AD resolves as children age in about 50-70% of cases.  The ultimate cause of AD is unknown, but it is often associated with other atopic features such as hayfever, allergies and asthma, and in many cases there is a genetic predisposition.  Eczema is impacted by a number of intrinsic and extrinsic factors, such as family history, environmental changes, overwashing, contact irritants and possibly dust mites.  It is well recognized that AD patients have very dry skin as part of their clinical picture.  As such, a very important part of discussing the treatment of AD includes the importance of moisturizing the skin on a regular basis to try to ameliorate dryness.

What changed my practice

The epidermis is often conceptualized as a brick wall, with keratinocytes forming the bricks and the intracellular lipids forming the mortar that holds the bricks together. For many years it has been thought that inflammation in the dermis leads to disruption and breakdown of the epidermal barrier. This inflammation was thought to stem from the genetic predisposition of these AD patients. There is new (and older) data that suggests the initial site of abnormality is within the epidermis itself, with primary barrier dysfunction then allowing penetration of allergens, irritants etc which sets up the inflammatory cascade that ultimately makes things worse.  We know that about 50% of patients with AD have a genetic mutation that reduces their levels of filaggrin in the epidermal layer.  Breakdown products of filaggrin create “Natural Moisturizing Factor”, made up of proteins, acids and humectants that help hydrate the skin. In patients without filaggrin, such as ichthyosis and AD patients, the lack of ability to self moisturize worsens the epidermal barrier dysfunction. The old hypothesis is called the inside-out theory, the new is the outside-in theory. It is likely that there is some element of truth to both of these theories and they may work in concert.

There are now on the Canadian market a number of “skin barrier repair” creams which aim to replenish the normal constituents of the intracellular lipid and try to fix the epidermal barrier. These creams are different than that of regular moisturizers or emollients, which serve to seal moisture into the skin and form only a physical barrier. These skin barrier repair creams have various concentrations of ceramides, cholesterol and free fatty acids, which are the components of the intracellular lipid matrix. Some of these lipids are incorporated into keratinocytes and excreted back out into the intracellular space, to fix the brick wall mortar.  It is unclear exactly what concentration of which lipid is most important and there are a number of products all with very different ingredients and percentages.  As such, there is no consensus and we are left with some degree of buyer beware. Skin barrier repair creams are available both in prescription (Epiceram cream) and over the counter preparations (CeraVe cleanser, lotion and cream, Cetaphil Restoraderm cleanser and lotion).

A randomized investigator-blinded study in 2009 compared Epiceram to a low-mid-potency topical steroid cream (fluticasone proprionate 0.05%) BID in 121 moderate to severe AD patients over 28 days. The results showed a similar degree of reduction (~50%) of itch, improvement in specific AD scores and improved sleep habits when looking at both arms of the study. Also, fewer patients in the Epiceram arm required steroid rescue therapy, making it a potential for monotherapy.  Another study in 2011 looked at Epiceram as monotherapy or in combination with various topical steroids.  Of the 207 patients, 54% were clear or almost clear at week 3, in either arm, especially those with mild AD.

CeraVe published in 2008 the use of its cleanser and moisturizing cream in 60 patients with mild to moderate AD. The products were used as adjuvant therapy BID with topical fluocinonide cream 0.05% to see if CeraVe could reduce AD symptom duration. Indeed, the addition of the CeraVe products did increase disease clearance from 15%  (with a mild bar soap, no mositurizer and steroids alone) to 76% (when steroids were used in conjunction with the CeraVe cleanser and cream). There are no similar studies for Cetaphil Restoraderm.  Remember also, these studies are small and not powered for non-inferiority, so results should be interpreted cautiously.

What I do now

Counselling is a significant component of treating AD.  I have always recommended lukewarm, short baths or showers, minimal use of mild cleansers and liberal use of creamy moisturizers.  Now, if I have a patient with AD who is doing all of those things to the best of their ability (and remember, they need regular reminders), I will suggest they try one of the new skin barrier repair creams. These can be used liberally all over or in hot spot areas that always tend to flare.  If a patient has a moisturizer that they like and tolerate, I will not suggest switching, but if they are looking for something new to try, have ongoing xerosis in spite of their moisturizer or aren’t using anything, these are good topical preparations to try. These topicals are only part of the treatment regimen we use when managing AD patients, but a newer tool that may give significant benefit, especially when used in conjunction with active medical therapies.

References

1. Thomas R, Landells I, Lynde C, Withers M et al. Canadian Consensus of Skin Barrier Therapy and Atopic Dermatitis. J Cut Med Surg 2012;16:S1-16.
2. Danby SG, Cork MJ. A new understanding of atopic dermatitis: the role of epidermal barrier dysfunction and subclinical inflammation. J Clin Dermatol 2010;1:33-46
3. Sugarman JL, Parish LC. Efficacy of a lipid-based barrier repair formulation in moderate-to-severe atopic dermatitis. J Drugs Dermatol 2009;8:1106-11

Dr. Mary V. Seeman (biography and disclosures)

What care gap I’ve noticed

Most practice guidelines for the treatment of schizophrenia are written with men in mind, ignoring the expanding research base that points to several important differences between the experiences of men and women who suffer from this illness (1).

Data that should be considered

1. Male/female differences in schizophrenia

Throughout the world, males begin their struggle with schizophrenia during adolescence, several years, on average, before women. This may be because men are exposed to more antecedents such as difficult pregnancies (male infants have more trouble in the womb than female infants), difficult deliveries (more obstetrical problems with male infants), early physical trauma (more rough and tumble play), more childhood psychiatric problems (autism spectrum, attention deficit disorder), more communication problems (speech defects, stuttering, slower language acquisition), more learning difficulties (2), more exposure to alcohol, drugs, and industrial solvents in their teens.

Consequent to an early illness start, males are frequently unable to complete their schooling or to experience romantic partnerships or to become independent of their parents before serious symptoms make all this impossible, or, at least, very difficult (3). Perhaps for these reasons, men respond less well to standard schizophrenia treatment than women, more often commit suicide during the first decade of illness, are more often aggressive and commit acts of lawlessness (4). Compared to women with schizophrenia, they are less often employed, less often enjoy an adequate social network, are less likely to look after their hygiene and health, and more likely to abuse alcohol and drugs.

However, there is improvement as men age. The aggression and denial of illness wane. They allow themselves to be cared for and, gradually, symptoms and quality of life improve. Paradoxically, women appear to do less well as they age. As their social supports decrease with the passage of time, adherence to medication also decreases and psychotic symptoms rise in severity, especially during and after menopause (5). Women previously free of illness develop psychotic symptoms for the first time at this age. Because women with a diagnosis of schizophrenia are not socially isolated, they can suffer the consequences of relatives and relationships – deaths, break ups, domestic violence, difficulties bringing up children, economic difficulties, frequent loss of child custody.

The trajectory of illness is, thus, different in women and men.

2.       Problems for the clinician

Because textbooks and guidelines are written from the male perspective [schizophrenia is slightly more prevalent in men than in women (6)], clinicians screening for schizophrenia look for teenagers who are withdrawn, hostile, uncommunicative and who exhibit bizarre behaviour. But women with schizophrenia present differently. They tend to be older, to have retained many of their premorbid social skills, to show their emotions, and to be capable of forming a therapeutic relationship. Despite the presence of psychotic symptoms, clinicians are loath to ‘label’ the illness schizophrenia because of the stigma that continues to attach to this illness. Women tend to receive the diagnosis of depression (because depression is so common in women) and to be treated with antidepressants, which not only exacerbates their psychotic symptoms but also delays effective treatment. This is unfortunate because early treatment has been shown to improve prognosis (7).

Clinicians also struggle with issues of sexuality, contraception, pregnancy, and parenting in the context of schizophrenia and women. These crucial subjects are neglected even though they are vital to the health of future generations.

Clinicians fail to recognize that psychotic symptoms can increase in women at certain times of the month (8) and at the time of menopause. Response to antipsychotic treatment can decrease at this time (9).

Clinicians may also fail to recognize that the side effects of antipsychotics differ in men and women (10).  In general, women require lower doses and develop more side effects. Weight gain, a common problem associated with antipsychotic medication, and its sequelae (diabetes and heart disease) are special problems for women.

What I recommend

1. Screen for psychotic symptoms in men and women of any age and prescribe antipsychotics whether or not prominent disturbances of mood are also present.
2. Take suicide precautions in schizophrenia, especially in younger men and older women (11).
3. Plan on improved outcome in men with schizophrenia as they age.
4. Discuss reproductive issues with both men and women and their families.
5. Be prepared to raise the dose of antipsychotic medication in women at menopause or change to depot formulations.
6. Antipsychotic medication can cause medically important side effects in both sexes (diabetes, cardiovascular disease and metabolic syndrome and these must be prevented or mitigated (12). Prevention can take the form of keeping doses low, selecting antipsychotics less prone to causing obesity, engaging patients in nutrition education and fitness programs, or adding medication that is safe in schizophrenia and that keeps weight down.

When general practitioners encounter young adults who are unable to concentrate, who have difficulty making themselves understood, who appear to be preoccupied with extraneous stimuli, who are isolated from friends and alienated from family, they should recommend psychiatric assessment for early psychosis. Mood disturbance with psychotic features may turn out to be the more accurate diagnosis but low dose antipsychotic medication will, whatever the diagnosis, calm the patient, ease the distress, and allow for the development of a therapeutic relationship. The focus of this article is to point out that men and women, regardless of diagnosis, usually have different service needs (13).

References (Note: Article requests might require a login ID with CPSBC or UBC)

1. Abel KM, Drake R, Goldstein JM.: Sex differences in schizophrenia. Int. Rev Psychiatry. 22(5), 417-428 (2010). (View with CPSBC or UBC)
2. Kirchengast S, Hartmann B.: The male disadvantage hypothesis reconsidered: is there really a weaker sex? An analysis of gender differences in newborn somatometrics and vital parameters. J. Life Sci. 1(1), 63-71 (2009). (View article)
3. Rabinowitz J, Levine SZ, Häfner H.: A population based elaboration of the role of age of onset on the course of schizophrenia. Schizophr. Res. 88(1-3), 96-101 (2006). (View with CPSBC or UBC)
4. Kao YC, Liu YP.: Effects of age of onset on clinical characteristics in schizophrenia spectrum disorders. BMC Psychiatry. 10:63 (2010). (View article)
5. Seeman M.V.: Treating schizophrenia at the time of menopause. Maturitas. 72 (I2), 117-120 (2012 ). (View article with CPSBC)
6. McGrath J, Saha S, Chant D, Welham J.: Schizophrenia: A concise overview of incidence, prevalence, and mortality. Epidemiol Rev. 30(1), 67-76 (2008). (View article)
7. Riecher-Rossler A.: Early detection of schizophrenia psychoses in men and women. Ther. Umsch. 64(6), 337-343 (2007).
8. Bergemann N, Parzer P, Runnebaum B, Resch F, Mundt C.: Estrogen, menstrual cycle phases, and psychopathology in women suffering from schizophrenia. Psychol. Med. 37,1427-1436 (2007). (Request from CPSBC)
9. Seeman MV.: Parenting issues in mothers with schizophrenia. Curr. Women’s Health Rev. 6(1), 51-57 (2010).
10. Seeman MV.: Secondary effects of antipsychotics: Women at greater risk than men. Schizophr. Bull. 35(5), 937-948 (2009). (View article)
11. Hor K, Taylor M.: Suicide and schizophrenia: a systematic review of rates and risk factors. J. Psychopharmacology. 24(4 Suppl), 81–90 (2010). (View article)
12. De Hert M, Correll CU, Cohen D.: Do antipsychotic medications reduce or increase mortality in schizophrenia? A critical appraisal of the FIN-11 study. Schizophr. Res. 117(1), 68-74 (2010). (View with CPSBC)
13. Scheyett AM, McCarthy E.: Women and men with mental illnesses: Voicing different service needs. Affilia. 21(4), 407-418 (2006). (Request from CPSBC)

How to Offer Better Support to Parents of People with Schizophrenia

by Susan Inman, BA, MA (biography)

What has been happening

Because too little accurate information about schizophrenia is available in popular culture and elsewhere, parents of people who develop this disorder experience enormous distress and are confused about what they should do. Many programs training mental health professionals do not provide science based curriculum about psychotic disorders and parents’ early interactions with various kinds of therapists can actually be harmful both to their child and to them. When therapists have only been trained in psychodynamic theories, not only can they fail to make appropriate referrals to early psychosis intervention programs, but they can lead families to believe that these neurobiological disorders have been caused by poor parenting.

What can change the lives of these parents

Providing accurate information about the state of knowledge about these disorders can help parents recover from the unjustified and demoralizing guilt they may have developed. When physicians become familiar with the kinds of help parents need, they can assist them in developing the behaviours that will lead to the best outcome for their child.

Five Tips for Helping Parents of persons with schizophrenia or psychotic disorders:
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Frequently Asked Questions

The use of sedation in end of life care has become a contentious issue because of concerns that, at the least, it may block the patient’s final opportunity to communicate either with his family or his God, and at worst may shorten life and be tantamount to covert euthanasia (1). In some settings there is evidence that this can indeed be the intention (2).

Why should sedatives be used as a palliative measure in terminally ill people? They are a last resort when a symptom is intractable, i.e. it cannot be controlled by any other means available. Note, that this means that intractability is contextual: it depends on the therapeutic resources that can be accessed and the physician’s capability to use them. Fewer symptoms require sedation if the doctor knows what he is doing and is prepared to try all the treatments first (3).

Data

Reports of the proportion of patients who require the use of sedatives in the closing days of life vary enormously, from 1% (4) to 88% (5). In large part this appears to reflect differences in definition of  the use of the word ‘sedation’, with some groups identifying only ‘continuous deep sedation’ which is intended to induce unconsciousness and maintain that state for the rest of the patient’s life, while others note every instance of the use of a sedative drug.

There is no doubt that a sedative dose high enough to cause respiratory depression can precipitate death. Six studies have examined survival times of patients given sedation in specialist palliative care settings. In five of them survival was the same or longer in those receiving sedatives as in those who had no sedatives (6). However, on average the actual duration of sedative use in palliative care is short. A review by Porta Sales of studies involving a total of over 1,700 patients found the mean duration of sedation to be 2.5 days (range 1.3-3.9 days) (7). In combination with the evidence of a lack of shortening of survival under a palliative care service through the use of sedatives, this suggests that sedation is generally a response to symptoms associated with the onset of dying.

Contrary, perhaps, to popular assumption, sedation is not often needed for intractable pain. By far the most common reason for its use in palliative care is agitated delirium, a situation that arises commonly at the end of life when no remediable cause can usually be found. The second most common indication is distress from severe breathlessness (8).

Worldwide, midazolam by subcutaneous injection or continuous infusion is the most often used drug for palliative sedation. Individual doses vary widely according to need, but the largest study has reported a median of 23mg/24h (9). Different  benzodiazepines, phenothiazine and other sedating antipsychotic drugs and, occasionally, phenobarbitone are also used, but opioids are inefficient sedatives and are inappropriate for this indication.

Practice tip

The keys to an ethically defensible use of sedation in palliative care are, firstly, careful assessment to determine whether the causes of the distressing symptoms can be reversed and, secondly,  the use of sedative doses that are proportional to the severity of the distress.  This issue of proportionality has been widely emphasised in recent literature and guidance in this area from Canada and elsewhere (10). The use of sedative drugs is analogous to the use of opioids for pain: a low initial dose is titrated higher against the response until distress is relieved. It is worth recalling that the root of the word ‘sedation’ is not the Latin for ‘sleep’ but for ‘soothing’. The primary intention should not be to achieve a certain level of reduced consciousness but to soothe the distress that is being felt and that cannot be eased any other way. It is not often that induction of coma is necessary for palliation, but a tired, ill patient may well fall asleep if they are at last made comfortable. Even without sedation, only 70% of terminally ill people are spontaneously awake a week before death, a proportion that falls to less than 25% by the last 72 hours of life (11).

Wherever possible, decisions about sedation should not be taken alone but arise out of multiprofessional discussion that should also involve the patient and family where this is practicable (12). It needs to be clearly documented that alternatives to sedation have been considered and that all available expertise has been brought to bear, particularly if sedation is being considered for psychological distress in a patient who is not imminently dying. In this situation an anxiolytic may be regarded as a specific treatment when set within a wider therapeutic approach, but any extended period of sedation needs very careful justification (13).

The provision of clinically assisted hydration or nutrition is a separate decision from that of sedation. The proportionate use of sedatives does not necessarily stop patients eating or drinking, but many patients in whom it is necessary are already taking little if anything by mouth as a result of their progressive illness and there is no clinical benefit in providing them with an infusion or feeding tube. However, the fact that sedation is being used should not in itself be taken as justification for stopping or withholding such interventions.

Sedatives are an intrinsic part of the armamentarium of palliation at the end of life, but they must be used in a considered way, taking alternative treatments into account, choosing an appropriate drug and adjusting the dose carefully to achieve comfort with the least necessary alteration of conscious level. Employing this approach, sedation allows a merciful easing of distress, it is a myth that it routinely shortens life  and so it is not a euphemism for euthanasia.

References (Note: Article requests might require a login ID with CPSBC or UBC):

1. Billings, JA., Block, SD. (1996) Slow euthanasia. J Palliat Care, 1996; 12(4):21-30. (View Article with UBC)
2. Rietens JA, van der Heide A, Vrakking AM, Onwuteaka-Philipsen  BD, van der Maas PJ, van der Wal G. Physician reports of Terminal Sedation without Hydration or Nutrition for Patients nearing death in the Netherlands. Ann Int Med, 2004; 141: 178-185. (View Article with UBC or CPSBC)
3. Morita, T., Akechi, T., Sugawara, Y., Chihara, S. and Uchitomi, Y. Practices and attitudes of Japanese oncologists and palliative care physicians concerning terminal sedation: a nationwide survey. J Clin Oncol, 2002;  20(3):758-64. (View Article)
4. Fainsinger, RL. Use of sedation by a hospital palliative care support team. J Palliat Care, 1998; 14(1):51-4. (View Article with UBC or CPSBC)
5. Turner, K., Chye, R., Aggarwal, G., Philip, J., Skeels, A. and Lickiss, JN. Dignity in dying: a preliminary study of patients in the last three days of life. J Palliat Care, 1996; 12:7-13. (View Article with UBC )
6. Sykes NP. Clinical Aspects of Palliative Sedation. In: Sterckx S, Raus K, Mortier F. Sedation at the End of Life. Cambridge: Cambridge University Press (in press).
7. Porta Sales, J. Sedation and terminal care. Eur J Palliat Care; 2001 ; 8: 97-100.
8. Fainsinger, RL., Waller, A., Bercovici, M., Bengston, K., Landman, W., Hoskings, M., Nunez-Olarte, JM. and deMoissac, D. A multicentre international study of sedation for uncontrolled symptoms in terminally ill patients. Palliat Med, 2000; 14(4):257-65. (View Article with UBC or CPSBC)
9. Sykes, N, Thorns, A. Sedative use in the last week of life and the implications for end-of-life decision making. Arch Intern Med, 2003; 163(3):341-4. (View Article)
10. Dean, MM., Cellarius, V., Henry, B., Oneschuk, D. and Librach, SL. Framework for Continuous Palliative Sedation Therapy in Canada. J Palliat Med, 2012; 15:870-9. (View Article with UBC)
11. Kohara, H., Ueoka, H., Takeyama, H., Murakami, T. and Morita, T. Sedation for terminally ill patients with cancer with uncontrollable physical distress.  J Palliat Med; 2005: 8:20-25. (View Article with UBC or CPSBC)
12. Nambisan V, Providing evidence of intention when giving palliative sedation. Eur J Palliat Care, 2012; 19: 93-96. (View Article with UBC)
13. Cherny NI, Radbruch L. (Board of the European Association for Palliative Care). European Association for Palliative Care (EAPC) recommended framework for the use of sedation in palliative care. Palliat Med, 2009; 23(7):581-93. (View Article with UBC or CPSBC)

What I did before

Most of us recognize that the world is increasingly connected and that infectious diseases know no borders. We are aware that returning travellers, refugees and immigrants can present with illness related to a tropical disease or parasitic infection acquired outside of Canada. However, we are not always pro-active in adequately screening our patients for these infections.

Although an elevated eosinophil count has long been recognized as a key diagnostic clue of a parasitic infection, it is often overlooked.

What changed my practice

A recent case of eosinophilia and Strongyloides hyperinfection and new screening guidelines from both Canadian¹ and US² expert groups have influenced my practice.

The case

Mr. L. is 46 years old, immigrated to Canada from Vietnam in 1992, and was previously in very good health.  This past September, progressively worsening headaches led him to seek medical attention at the emergency department where a CT scan was done and showed evidence of brain metastases from a lung primary. He was started on high dose dexamethasone and referred for bronchoscopy and further oncological management. His routine blood work was normal apart from an elevated eosinophil count – which was overlooked.
Over the next few days to weeks, on steroids, his headaches improved, but he began to feel itchy.  His first bronchoscopy was non-diagnostic.  His repeat bronchoscopy confirmed lung cancer, and the microbiology technician observed an unusual pattern in the normal respiratory bacteria growing on the petri dish – some of the bacterial colonies were spread out in linear tracks. This was an incidental finding, but, to the trained eye, was characteristic of the presence of Strongyloides larvae. Further testing confirmed that Mr. L. had Strongyloides hyperinfection, a potentially fatal disease if not treated early.

Strongyloides stercoralis larva tracks on a blood agar plate from the bronchoalveolar lavage of a patient with disseminated strongyloidiasis (taken from Sue Lim et al.³)

Strongyloides is endemic throughout most of the world, especially tropical, sub-tropical, and developing countries.  Asymptomatic strongyloidiasis can persist for decades after immigration.  Eosinophilia, a useful indicator, is not always present.  If left untreated, in the setting of immunosuppression with even relatively short courses of steroids, it can result in severe illness or death through disseminated disease.

Mr L. had acquired Strongyloides infection years ago in Vietnam.  Other than his elevated eosinophil count he was entirely asymptomatic.  Only when he was given steroids did the infection become symptomatic as the larvae began to replicate in very high numbers unchecked by his suppressed immune system.  Fortunately, he was diagnosed in time and did well following treatment with ivermectin.

The guidelines

The Canadian Collaboration for Immigrant and Refugee Health (CCIRH) recommends screening all refugees arriving from countries in Africa or South East Asia for strongyloidiasis using serology.¹  Additional serology for schistosomiasis is recommended for those from Africa.

The US Centre for Disease Control (CDC) and the Division of Global Migration and Quarantine recommend serological screening for strongyloidiasis for all refugees regardless of region of origin.²  In addition, they recommend that all refugees are screened with a CBC (looking for eosinophilia) and stool O&P examination. Schistosomiasis serology is also recommended for refugees from Sub Saharan Africa.

What I do now

In view of the prevalence of parasitic infections among refugees, and the extremely high mortality rate of disseminated strongyloidiasis, I support comprehensive screening for eosinophilia, stool O&P examination, and Strongyloides serology for all refugees, especially those from Africa or South East Asia.

I consider serologic screening for Strongyloides mandatory for all patients who have a history of residence in a tropical or sub-tropical country and require immunosuppressive therapy (corticosteroids, transplant, or chemotherapy).

I interpret an elevated eosinophil count as a parasitic infection until proven otherwise and I pursue comprehensive investigations, tailored to the patient’s epidemiological history, in my diagnostic approach.⁴

Serology for Strongyloides can be drawn at any outpatient laboratory and will be forwarded to the national reference laboratory in Montreal for testing. Unlike stool examination, serology has excellent sensitivity for the detection of Strongyloides infection.

Ivermectin is the treatment of choice for strongyloidiasis. However, along with albendazole, it is not available in pharmacies and must be obtained through the Special Access Programme. Instructions on how to obtain these medications can be found at Health Canada’s website.⁵

Providing care for immigrants and refugees requires attention to their previous experiences with the health care system, the potential lack of prior access to preventive care and exposures to infectious diseases.  The CCIRH guidelines provide evidence-based recommendations to help guide our practice.¹

Not all parasitic infections require international travel or visits to tropical countries.  Important, not to be missed, parasitic infections can be acquired right here in BC.  For example, raccoon roundworm (Baylisascaris procyonis), a cause of potentially fatal encephalitis is common in raccoons and a potential, albeit very rare, risk to children throughout most of Canada.⁶

Patients with unexplained eosinophilia or parasitic infection can be referred for consultation to the tropical medicine clinic at the Diamond Centre, Vancouver General Hospital. Our fax number is (604) 874-4013.

What I did before

Thyroid nodules found on physical examination are common. It is estimated that up to 7% of adults in the United States have a palpable thyroid nodule (1). Fewer than 5% of these nodules are malignant (2). In accordance with the most recent guidelines of the American Thyroid Association (3), I obtain a TSH in patients with a thyroid nodule. If the TSH is low, the patient should be investigated for hyperthyroidism using a radioactive iodine scan. In absence of any worrisome features on history or physical exam (Table 1), a hyper functioning nodule on a scan has a very low probability of being malignant (4). However, patients with palpable nodules and normal or high TSH require an ultrasound and a great deal of useful information can be gained from the imaging.

Fine needle aspiration (FNA) of the thyroid nodule should be performed under ultrasound guidance in all patients with nodules of >1 cm or in patients with features on history, physical examination, or ultrasound which suggest an increased risk of malignancy (Tables 1 and 2) regardless of nodule size. While some FNA’s will definitely be benign and some positive for thyroid cancer – in which case patients should be referred to a surgeon for removal.  Approximately 15-30% of FNA’s will yield indeterminate results (3). These indeterminate findings are one of “atypia (or follicular lesion) of undetermined significance,” “follicular neoplasm or suspicious for follicular neoplasm,” and “suspicious for malignancy” (5, 6).

Indeterminate results present a diagnostic dilemma: based on history (see Table 1) and other ultrasound or pathological findings, some patients are referred for surgery while others are monitored. It is inevitable that some patients with indeterminate results may undergo surgery and be found to have benign pathology.  However, the rate of unnecessary surgery can be reduced using ultrasound and genetic tools.

What changed my practice

Ultrasound can be a powerful tool in distinguishing thyroid nodules with malignant potential from benign ones. I look for the ultrasound to answer the following questions: 1) How many nodules are there and how big is each one? 2) Is the nodule a simple cyst? 3) Is there increased vascularity? 4) Are there micro calcifications in the nodule? 5) Is the nodule hyper/hypo-echoic? 6) Is the lesion taller than wide on transverse view? 7) Is there suspicious cervical lymphadenopathy?

Numerous studies have evaluated predictive value of ultrasound findings in determining malignant features. In a study done by Bastin et al (8), microcalcifications were 84% and ill-defined or lobulated margins were 89% specific for nodules associated with thyroid cancer.  A recent review article, in World Journal of Surgery, identified features that have been consistently found to be significantly associated with malignancy (9).  Thus, these ultrasound characteristics can be very useful in making decisions about surgery in patients with indeterminate cytology.

Gene mutations can be identified in 60-70% of cases of thyroid cancer (7).  Genetic testing on FNA samples shows promise in further characterizing thyroid nodules that have indeterminate FNA results. In August 2012, Alexander and colleagues (10) reported their findings on using Afirma® Gene-Expression Classifier (Veracyte©) in pre-operative diagnosis of thyroid nodules with indeterminate cytology. The gene-expression classifier used 167 genes to classify the aspirated material. Of the final 265 indeterminate fine-needle aspirates used in the analysis, based on histopathological review, 85 (32%) were identified to be malignant. The gene-expression classifier correctly identified 78/85 of the samples as “suspicious” (sensitivity 92%, 95% Confidence Interval [CI], 84-97). Conversely, of the remaining 180 samples, 93 were correctly identified to be non-malignant by the assay (specificity 52%, 95% CI, 44-59).  This corresponded to a negative predictive value (NPV) 93% (86-97) and a positive predictive value (PPV) 47% (40–55). Overall, the assay had 100% sensitivity (29-100) and 70% specificity for cytopathologically benign samples.

What I do now

Evaluation and work-up of a thyroid nodule is a relatively common presentation. I continue to follow the American Thyroid Association guidelines (3) in seeing these patients. It is nevertheless important, however, to have relevant radiological findings reported to aid in further management of these nodules (see above). Your ultrasound reports may not contain all of this information.  If they do not, talk to the radiologist as these ultrasound characteristics are very useful in determining risk of malignancy, especially in samples with indeterminate cytology. Application is being made to have molecular testing on FNA specimens be a funded service in British Columbia (personal communication, B. Gilks M.D., Department of Pathology, Vancouver General Hospital), and thus available for patients in BC. However, the use of molecular diagnostic techniques should be limited to those samples in whom history, physical, and detailed ultrasound analysis do not provide sufficient information to guide surgical management.  Additional note: There is not a role for nuclear scanning in the evaluation of thyroid nodules in the euthyroid patient.  The nuclear scan will show a nodule as being hot, normal or cold.  If the nodule is hot, it is unlikely to be malignant but if the nodule is hot, the TSH will be suppressed.  While cold nodules are more likely than normal nodules to be malignant, most cold nodules are benign and not all malignant nodules are cold.  Thus, the nuclear scan has little discriminatory power.

References (Note: Article requests might require a login ID with CPSBC or UBC):

1. Singer PA, Cooper DS, Daniels GH, et al. Treatment guidelines for patients with thyroid nodules and well-differentiated thyroid cancer. American Thyroid Association. Arch Intern Med. 1996;156(19):2165-72. (View article with CPSBC or UBC)
2. Wong CKM, Wheeler MH. Thyroid nodules: rational management. World J Surg. 2000;24:934-41. (View article with CPSBC or UBC)
3. Cooper DS, Doherty GM, Haugen BR, et al. Revised American Thyroid Association management guidelines for patients with thyroid nodules and differentiated thyroid cancer. Thyroid. 2009;19:1167-214. (View article with CPSBC or UBC) [Erratum, Thyroid 2010;20:674-5.] (View article with CPSBC or UBC)
4. Hegedus L. Thyroid Nodule. N Eng J Med. 2004;351:1764-71. (View article with CPSBC or UBC)
5. Baloch ZW, Cibas ES, Clark DP, et al. The National Cancer Institute thyroid fine needle aspiration state of the science conference: a summation. Cytojournal 2008; 5:6. (View article)
6. Cibas ES, Syed AZ. The Bethesda Sys- tem for reporting thyroid cytopathology. Am J Clin Pathol. 2009;132:658-65. (View article with CPSBC or UBC)
7. Moses W, Weng J, Sansano I, et al. Molecular testing for somatic mutations improves the accuracy of thyroid fine- needle aspiration biopsy. World J Surg. 2010;34:2589-94. (View article)
8. Bastin S, Bolland MJ, Croxson MS. Role of ultrasound in the assessment of nodular thyroid disease. J Med Imaging Radiat Oncol. 2009;53(2):177-87. (View article with CPSBC or UBC)
9. Morris LF, Ragavendra N, Yeh MW. Evidence-based assessment of the role of ultrasonography in the management of benign thyroid nodules. World J Surg. 2008;32(7):1253-63. (View article with CPSBC or UBC)
10. Alexander EK, Kennedy GC, Baloch ZW, et al. Preoperative diagnosis of benign thyroid nodules with indeterminate cytology. N Engl J Med. 2012;367:705-15. (View article with CPSBC or UBC)

What frequently asked question I’ve noticed

Acute limping is a very common chief complaint among children visiting a clinic or an emergency department [1]. The main differential diagnosis includes arthritis (viral or bacterial), osteomyelitis, Legg-Calve-Perthes disease (idiopathic avascular necrosis) and slipped capital femoral epiphysis.

One of the most common reasons for acute limping is Transient Synovitis, also named ‘A-septic Arthritis’ [2]. This condition, representing a viral infection in a large joint, is most common between 3 and 10 years of age, with a mean age of 6 years. It occurs more frequently in boys and in vast majority of cases is unilateral (>90%).

Children are usually symptomatic for 24-48 hours before their parents seek advice from a health care provider. They may limp or not bear weight on the affected leg. They may have a low grade fever, albeit most patients are a-febrile. The hip is the most common joint involved in the process.

One of the key elements in illness history, that help with the diagnosis of transient synovitis, is the description of a preceding viral illness, usually 2 to 3 weeks prior to their presentation [3].

While transient synovitis is a very benign condition that will resolve spontaneously in a few days, and is treated with analgesia, it may be confused with a much more severe condition – Septic Arthritis – a bacterial infection. The importance in differentiating between the two conditions is the fact that septic arthritis will necessitate an immediate action for diagnosis (tapping the joint) and treatment (IV antibiotics and admission).

Data that answers this question

So how can one differentiate between transient synovitis and septic arthritis?

Clinical exam – this is the most important differentiator. Children with septic arthritis look sick. They are unwell, tired, possibly lethargic and will do very little activity. With transient synovitis, parents may report limping as the only ‘new’ finding, as the child will likely be active, alert, feed and in general – will look well.

Physical examination – Examination in young, non-cooperative children, is always challenging. When the child is cooperative, he or she may have limited range of motion (mostly internal rotation of the hip), and with septic arthritis children will usually be guarding their joint and avoid movement as much as they can.

Plain x-ray of the hip – similar to clinical and physical exam, a plain x-ray may not be as beneficial in distinguishing between the two diagnoses, as evidence of some effusion and widening of the joint space may be evident in both conditions.

Blood tests – In transient synovitis the white blood cells count, differential count, sedimentation rate (ESR) and other inflammatory markers (CRP) are usually within normal limits, while in septic arthritis they are usually elevated. This differentiation however may not be evident in the first few days of illness, and normal counts should not be used as a measure to rule-out septic arthritis. Procalcitonin [4] has not been shown to be of benefit in differentiating the conditions.

Prediction rule [5] – In an effort to provide a combined diagnostic test for septic arthritis (of the hip), four independent predictors (history of fever, no weight-bearing on exam, ESR of 40 mm/hr, and a serum white blood cell count of >12,000 cells/mm(3)) were identified and validated as a reliable measure.

Practice tip in managing this problem

When children with a limp present to you, always consider the possibility of septic arthritis. The key element in deciding on tapping the joint, referring to an emergency department or an orthopedic surgeon or ordering an ultrasound is the clinical presentation of the child. When in doubt or if there is no good follow-up available – draw blood work, and order a plain x-ray of the joint. Give ibuprofen to relieve the pain and reassess the child after 20-30 minutes as limping and pain from transient synovitis should improve. When the child looks unwell – an urgent tapping of the joint and systemic antibiotic therapy is needed.

References / Additional reading (Note: Article requests might require a login ID with CPSBC or UBC)

1. Krul M, van der Wouden JC, Schellevis FG, van Suijlekom-Smit LW, Koes BW. Acute non-traumatic hip pathology in children: incidence and presentation in family practice. Fam Pract. 2010;27(2):166-170 (View article)
2. Fischer SU, Beattie TF. The limping child: epidemiology, assessment and outcome. J Bone Joint Surg Br. 1999;81(6):1029-1034 (View article)
3. Kastrissianakis K, Beattie TF. Transient synovitis of the hip: more evidence for a viral aetiology. Eur J Emerg Med. 2010;17(5):270-273 (View article with CPSBC or UBC)
4. Butbul-Aviel Y, Koren A, Halevy R, Sakran W. Procalcitonin as a diagnostic aid in osteomyelitis and septic arthritis. Pediatr Emerg Care. 2005;21(12):828-832 (View article with CPSBC or UBC)
5. Kocher MS, Mandiga R, Zurakowski D, Barnewolt C, Kasser JR. Validation of a clinical prediction rule for the differentiation between septic arthritis and transient synovitis of the hip in children. J Bone Joint Surg Am. 2004;86-A(8):1629-1635 (View article with CPSBC or UBC)

Statistics Canada ¹ reports that more than ¼ of Canadians are obese.  When those classified as merely overweight are included, 44.2% of women (5.6 million) and 60.1% of men (7.6 million) are deemed to be at risk for health consequences.  Among the risks associated with excess weight are important chronic diseases such as type 2 diabetes, hypertension, cardiovascular disease, osteoarthritis and some cancers.

BC Guidelines ² recommend lifestyle management as first line intervention.  Achieving and maintaining a healthy body weight is an important objective for patients and physicians alike.  Physicians of normal weight may be more likely to provide recommended obesity care to their patients and to feel confident in doing so; ³ and patients may be more likely to take their advice. ^{4, 5}

What I did before

Years ago, I found Weightwatchers groups to be a great patient resource – before they started flogging ‘product’.  Regardless, group programs and nutritionists are not available in all communities, and most people can’t afford a personal fitness and diet coach.

This app changed my practice

Just in time for New Year’s resolutions, here’s an app to recommend to your patients and, perhaps, to make use of yourself.

If we want to lose weight we need to consume fewer calories than we burn.  Learning how to do that is HARD – but it’s a lot easier with some handy computing power.  Based on the principle that keeping track of what we do helps modify or affirm our behaviours, My Fitness Pal www.myfitnesspal.com offers a relatively easy method of maintaining a balance sheet on that simple but elusive equation: what goes in, must come out (in a metabolic sense that is).  By my reckoning, My Fitness Pal meets BC Guidelines criteria that weight loss programs should encourage regular physical activity; be based on a balanced diet of e.g. 500-1000 kcal/day deficit; support an initial weight loss goal of 5-10% of the original weight; and recommend a rate of loss of no more than 0.4-1 kg (1-2 lb) per week.²

My Fitness Pal (MFP) bills itself as a calorie counter, diet and exercise journal.  There are mobile apps for iPhone, Android, Blackberry and Windows phones, for iPad, and also an option rich website.  Membership is free, as are the apps.

My Fitness Pal

Here’s how it works:

Create an account (you can use a pseudonym).  Be guided through creating your profile: weight, height, age, background activity level; then enter your exercise and weight loss (or weight gain) goals.  MFP calculates a recommended daily caloric intake “Goal” for you.

Now start entering everything you eat, and the cardiovascular exercise you do each day.  MFP makes it easy to do this in real time, with a searchable food database touted as holding 2.25 million food and restaurant items.  Entries you make on your phone will synchronize with your web account and vice versa.  The bar code scanner (on the iPhone app anyway) makes searching new items even easier.  Likewise, there’s a cardiovascular exercise database.

To make food entries, simply search the MFP database or your own past entries (which can be sorted by Recent or Frequent categories).  Create shortcuts with My Foods, Meals or Recipes.  Modifying quantities is also easy.  You had a large latte yesterday, but a small one today? Walked 30 minutes last night at a moderate pace, but only managed 20 minutes leisurely stroll today?  MFP calculates the calories (consumed or burned) from the food weight/volume or exercise duration entered.  The first week on MFP is more time-consuming because you are developing a database of your most common foods.

By monitoring calories (in and out) throughout the day, you gain real-time feedback.  MFP displays how many calories you have left in your day (displayed in green) or if you’ve (literally) gone into the red on your goals. Along the way you learn what foods are your calorie culprits, and appropriate serving sizes become far easier to judge.  Do you really have room for that second helping?

The app is devoid of advertising (unlike the website. Remember, it’s free).

My Fitness Pal

What I do now

I recommend My Fitness Pal to my patients, with a brief demo and some tips:

• Keeping track can be very motivating.
• It gets easier to log, because the My Fitness Pal program remembers your foods and exercises.
• There are good FAQ and video tutorials.
• Make www.myfitnesspal.com the home page on your computer.
• Don’t obsess if you don’t find an exact food match.  The wrong brand of Oatmeal Stout Porter probably has about the same amount of calories as your brand.  (If you really want to, you can enter new foods (or brands) into the database using the website).
• You can choose fractions or decimals for adjusting portion sizes.
• The little “wrench” is used to remember a meal or copy it to another day.
• If you are achieving your daily calories balance but your weight isn’t changing as expected, then use a food scale and spoon/cup measures when it is convenient to do so.  Estimates are just fine, but measuring is helpful for learning portion sizes.
• If you want to follow your macro nutrient intake, note that Nutrition Fact labels are based on a 2000 calorie/day diet.  Also note that as many entries in the MFP database are “crowd sourced” and calories are the minimum user entry requirement, nutrient info may be missing.  Read the FAQs for more info.
• There is a large online MFP community that is completely optional.  There you’ll find some useful, and some misleading info as well.  I advise my patients to be careful, and sensible.
• DON’T click the ads!

I offer to weigh my patient, calculate BMI, measure waist circumference – and I write these down for them.  I also suggest a follow-up appointment in a couple of weeks.

I know of no systematic research into the efficacy of this app.  I can report positive anecdotal experience of patients, friends and myself.  The MFP program appears to meet BC Guidelines criteria ² for recommendation.

BC Guidelines: For information on the diagnosis and management of overweight and obese adults, see http://www.bcguidelines.ca/guideline_obesity.html

Billing: Diet and exercise modification counseling (if CVD risk) are among the targeted clinical prevention actions that can be incorporated into a patient plan following a Personal Health Risk Assessment. For details on how to bill G14066: http://www.gpscbc.ca/system/files/GPSC%20Prevention%20Initiative%20Billing%20Guide-Revised%202011.pdf  ⁶

I have no conflict of interest to declare.

As the holidays are upon us and we end another great year, I wanted to take an opportunity to once again thank our readers for their ongoing support and active participation in voting, commenting and claiming CPD credits.

Of course, thanks must be extended to our authors, editors and the great efforts of Ms Nina Zoric, our Educational Program Coordinator at UBC CPD.

Basically through word of mouth, we now have over 10,000 biweekly readers.  With each posting, we often have more comments than large, international, commercially-based medical news websites.

Our concurrence rate remains high: 74% of the time readers stated the would “likely” or “definitely” change their practice.

This year’s top 5 articles for concurrence:

Our crowning achievement this year was having the honor of receiving the 2012 Royal College Accredited CPD Provider Innovation Award. This was a great validation of our efforts and will serve as an additional inspiration to keep pushing forward.

In the coming year, we anticipate a few more changes at This Changed My Practice as we continue to evolve:

1. We’ve partnered with UBC Faculty Development to bring new articles on innovative teaching strategies, with a subset of articles called “This Changed My Teaching” http://thischangedmypractice.com/category/teaching/.
2. Expansion of content to include other universities and provinces.  We are working on ways to address regional resources for readers outside of BC.  Where possible, we try to link BC-based guidelines and resources to article — given our expanding readership, we’re exploring ways of doing this for other provinces.  We may also be featuring content from other universities (but always in the TCMP style of article).
3. For our Royal College fellows (specialists), we are working with the Royal College on a mechanism for automated transfer of CPD credits to your Mainport account.

Of course, if you have suggestions, or want to contribute to This Changed My Practice, please feel free to contact me at editor@thischangedmypractice.com.

On behalf of all of us at TCMP, best wishes for a safe, happy and healthy holiday season.

Steve Wong, MD, FRCPC
Clinical Associate Professor, Department of Medicine, UBC
Medical Director, Clinical Practice Reviews, UBC CPD
Medical Director, This Changed My Practice, UBC CPD

PLEASE NOTE:

NO CREDITS ARE GIVEN FOR THIS POSTING

Dr. Bill Gibson (biography and disclosure)

What I did before

To be honest, Direct-to-Consumer Genetic Testing (“DTC” Genetic Testing) wasn’t really on my radar until a patient showed up on my doorstep with a result in hand. Broadly speaking, I used to see three main applications for sequencing a large number of genes in a specific individual. The first application was for ancestral origin: looking at DNA sequences all over the genome to get a better idea of a specific person’s ancestry.  Because different bits of the genome map track back to different regions of the world map, we can get a rough idea of where someone’s historic (and sometimes prehistoric) relatives used to live. Medical applications of this approach seem pretty limited, so some genomicists call it “recreational genomics.”  It doesn’t really require full sequencing of the human genome, but many private sequencing providers offer it.  The second application is diagnostic: to find rare mutations that have a large effect on someone’s health. These rare mutations truly cause disease. Examples include connective tissue mutations (heart disease), mutations in muscle proteins (muscular dystrophy), certain cancers (e.g. breast cancer, ovarian cancer and colon cancer), mutations in deafness genes and mutations in brain-, eye- and nerve proteins (neurological disease and/or vision loss). These types of rare diseases are often caused by one or two major mutations in a gene, leading to dominant or recessive inheritance.  For some of them, any one among a large group of genes could harbour mutations, so a “one gene at a time” search becomes really long and expensive. In these situations, high-throughput sequencing can be a cost-effective way to get almost all of the genes in one go, letting us quickly find the type of mutation(s) we are looking for.  The third application was semi-predictive: to find common genes that have a small effect on someone’s health, but that may have a large effect on health when added (or multiplied) together. The hope behind this type of testing is that these sequences can be assembled into a profile that would have some ability to classify a person into “high-risk” or “low-risk” categories for common diseases, such as heart disease and stroke, diabetes, dementia, asthma and so forth.

What changed my practice

I was referred a patient who had paid privately for high-throughput DNA sequencing, and then had her genome interpreted by several specialists in the field. I was asked to decide whether a particular rare mutation explained a number of unusual features in her medical history. These features were consistent with a common disease, though many of her close relatives also had the same disease. Thus, the presence of a dominant gene in the family was another plausible explanation. Like the result of any test I might have ordered myself, the patient’s data might help me to do my job, but it wouldn’t do my job for me.  I therefore also looked at her family history, and it became clear that there was no way to be certain that this specific mutation was causing her health problems. We are now trying to get better evidence to match the gene with the disease by testing other family members for the same mutation found by the private genome sequencing company. We are not sequencing all of their genes, just the one area where the mutation is found. We can do this because we have a research lab, but this is beyond the scope of what many family docs could do in the clinic.

This case made me more skeptical about the current medical usefulness of DTC genetic testing for common diseases, whether it finds rare mutations or common variants. That third application now seems to be much more distant in the future.

What I do now

From the perspective of one’s own ancestry, DTC genetic tests can return data that is interesting, and sometimes surprising, but it is difficult to imagine a good rationale for changing medical management on the basis of ancestry. It must be remembered that the “family history” one learns from ancestry testing is not the same as the traditional “family history” that a family doc would collect as part of routine care.

From a medical perspective, I advise people who are thinking about DTC genetic testing to think of it like the over-the-counter (OTC) medical tests available in many pharmacies. An OTC pregnancy test is designed to answer a focused question: whether or not a woman is pregnant. An OTC cholesterol test answers a similarly focused question.  I tell people that DTC genetic tests very rarely return results that are medically actionable, unless originally done to answer a focused question about a rare genetic disease.

That said, most DTC genetic testing is still not well suited to detecting rare disease-causing mutations. Patients who have concerns about a specific genetic disease, or an unusual problem that may be genetic in nature, are best served by a referral to the Provincial Medical Genetics Program or to the BC Cancer Agency’s Hereditary Cancer Program. Though DTC genetic testing may uncover major mutations that cause cancer or other diseases, current methods “flag” a large number of rare DNA changes that aren’t really there (false positive mutations) and fail to flag an unknown number true mutations – thus generating false negative results. This makes it hard for a practitioner to know if the real mutation he or she is looking for will actually be found the list returned by the company. Targeted testing of specific candidate genes through a certified lab (such as the Molecular Genetics Lab at Children’s and Women’s Health Centre of BC) offers the highest sensitivity and specificity in the context of rare genetic diseases.

Although DTC genetic tests can return a “panel” of common DNA sequences that match up some of the time with common diseases, these “panels” don’t reliably tell you who will get sick, when they will get sick, or how sick they will get. A multi-generation family medical history (three generations if known) remains the gold standard to assess risk for common diseases; DTC genetic testing doesn’t yet do better than that.

Being a Careful Consumer – A Checklist:
Practitioners who are asked by a patient about DTC genetic testing may suggest that the patient consider the following points:

1. What do you really want to find out from the test?

Ancestry tests can be fun and interesting, but should not be confused with tests that yield medically actionable information. If the patient is seeking a definitive diagnosis for a condition such as chronic pain, hormonal problems or other poorly-defined conditions, DTC testing is likely to raise more questions than it answers. If the patient is seeking a definitive diagnosis for a rare genetic condition, this is best pursued through their local Medical Genetics service.

2. How long has the company been doing DTC testing, and how many tests have they done?

There are many players in this field, and it is much easier for a company to generate DNA sequence data than it is to interpret it. Patients should avoid new start-up companies that appear to be cashing in on a trend.

3. Is the testing offered in a lab that abides by CAP- and CLIA-regulations?  

Patients may not know what the Clinical Laboratory Improvement Amendments or the College of American Pathologists are, but the lab should! Labs offering testing should comply with one or both of these. Labs outside of North America should have their procedures certified by an appropriate independent body.

4. Is the company doing the test itself, or is it acting as a “broker”?

Some companies collect the DNA and send it off elsewhere for sequencing. A careful consumer or GP should know where the testing is being done, and also what is the real “value added” by the company collecting the sample.

5. Who is actually doing the interpretation of the test?

Any test that is intended to be medically actionable should be signed out of the lab by someone with the legal authority to take responsibility for medical reports – like a pathologist, medical microbiologist, molecular geneticist, and so forth. It should not be a series of fields generated by a computer.

References and Further Reading:

Ashley E et al., “Clinical assessment incorporating a personal genome.” The Lancet, Volume 375, Issue 9725, Pages 1525 – 1535, 1 May 2010

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)60452-7/abstract

This group of authors suggest a way to start with population-prevalence data, throw in common DNA variants from whole genome sequencing and calculate an individual’s risk for developing common disease. Their algorithm generates a percentage risk, but the accuracy of this risk assessment (e.g. whether or not 10% of people who receive a 10% risk for type 2 diabetes from the calculation will actually go on to get type 2 diabetes) is not yet known.

Useful Websites to find out more:

UBC CPD Webinas:

BC Clinical Genomics Network

http://www.bccgn.ca

How to Make a Referral to the BC Cancer Agency Hereditary Cancer Program
(Site contains downloadable referral form)

http://www.bccancer.bc.ca/HPI/CancerManagementGuidelines/HereditaryCancerProgram/referralinformation/default.htm

How to Make a Referral to the Provincial Medical Genetics Program
(Site contains downloadable referral forms)

http://www.bcwomens.ca/Services/Medical+Genetics/ContactUs.htm

How to Order a Specific Genetic Test from BC’s Molecular Genetic Laboratory
(Site contains interactive test menu and downloadable requisition – please note that this lab does not offer direct-to-consumer genetic testing)

http://www.genebc.ca

Wikipedia

http://en.wikipedia.org/wiki/Genetic_testing#Direct-to-Consumer_genetic_testing

Genetics Home Reference

http://ghr.nlm.nih.gov/handbook/testing/directtoconsumer

American College of Medical Genetics and Genomics Statement on DTC Genetic Testing

http://www.acmg.net/StaticContent/StaticPages/DTC_Statement.pdf

What I did before
In the US, more than 200,000 patients are diagnosed with venous thromboembolism (VTE) events annually (1). Up to 30% of these patients die within 30 days (1). I manage all cases of diagnosed pulmonary embolism (PE) by initiating low molecular weight heparin (LMWH) (Dalteparin 200 IU/kg SC QD) or IV unfractionated heparin (UFH) (in patients with renal failure). Thereafter, following the CHEST guidelines (2), I start Warfarin on the second day, and ensure that the patient has at least 5 days of treatment with heparin, and their INR is in the 2-3 range for at least 2 days before continuing management with Warfarin alone.
There are challenges with use of Warfarin for treatment of VTE. The narrow therapeutic target may be difficult to achieve in some patients. Even within the same patient, depending on the diet and use of other concomitant drugs, there may be big swings in the weekly INR values. Patients, often limited by mobility and access to transportation, have challenges going to laboratory facilities for having their INR checked. There is also significant variability in physician comfort level for adjusting warfarin dosing leading to difficulties in maintaining therapeutic window.
However, the advent of new anticoagulation drugs is revolutionizing conventional treatment methods. One of these new anticoagulants is Rivaroxaban. Rivaroxaban is a potent Factor Xa inhibitor (3). With a rapid oral absorption profile, the drug reaches peak plasma concentration in 2.5-4 hours (4). Its half-life is 5-9 hours in healthy individuals and 9-13 hours in those older than 65 years old (5).

What changed my practice
In April 2012, NEJM published “The EINSTEIN-PE” (6) study, which looked at the use of oral Rivaroxaban for the treatment of symptomatic pulmonary embolism in 4833 patients. In a randomised, open-label, multicentre, non-inferiority international study with funding from Bayer Health-Care and Janssen Pharmaceuticals, study authors recruited patients with symptomatic PE with or without documented DVT. They excluded patients who were treated with LMWH or UFH for more than 48 hours, received fibrinolytics, had a thrombectomy, or placement of a IVC filter. Furthermore, they excluded patients with Creatinine Clearance of less than 30 ml/min or those who had liver impairment. Pregnant or breastfeeding women were also excluded from the study.
Patients in the study arm were randomized to receive Rivaroxaban 15mg BID for three weeks, and then to be switched to 20 mg daily. The control arm of the study treated patients with the “conventional method” of Enoxaparin 1 mg/kg BID with subsequent bridging to Vitamin K antagonists (VKA, Warfarin/Acenocoumarol) according to the CHEST guidelines. The period of anticoagulation was determined by the treating physician before randomization. Patients were followed up for the intended treatment period (3, 6 or 12 months).
Baseline characteristics of the study patients including extent of pulmonary embolism, cause of pulmonary embolism (provoked vs. unprovoked) and history of thromboembolism were similar between the two groups. The pulmonary embolism was thought to be unprovoked in approximately 64% of patients in both groups. Similar number of patients had active cancer in both arms (4.7% in Rivaroxaban arm vs. 4.5% in Standard treatment arm). Most patients in both groups were anticoagulated for 6 months (57.3% in the Rivaroxaban arm vs. 57.5% in the Standard therapy group). Furthermore, approximately 37% of patients in both arms received 12 months of anticoagulation treatment. Patients were followed for the length of the treatment. The primary outcome of the study was symptomatic recurrent VTE. The primary safety outcome was measured as clinically relevant (major and non major bleeding) bleeding.
In the 2419 patients who were assigned to receive Rivaroxaban, 50 (2.1%) patients had recurrent VTE when compared to 44/2413 (1.8%) who were treated with standard therapy (Hazard ratio 1.12, 95% confidence interval of 0.75-1.668; P=0.003 for one-sided non-inferiority margin of 2 and P=0.57 for superiority). There was no statistically significant difference between the two groups in terms of first episode of major or clinically relevant non major bleeding (10.3% in Rivaroxaban arm vs. 11.4% in standard treatment arm, hazard ratio, 0.9; 95% CI 0.76-1.07;P=0.23). However, there were 26 (1.1%) episodes of major bleeding in patients treated with Rivaroxaban compared with 52 (2.2%) in the standard treatment arm (hazard ratio, 0.49; CI 0.31-0.79, P=0.003).
Authors concluded that in patients with symptomatic PE, oral Rivaroxaban alone is non-inferior to Warfarin for preventing reoccurrence of VTE, with the possibility of an improved safety profile.

What I do now
Based on the data presented above, Rivaroxaban can be considered equivalent to Warfarin for management of patients with a new diagnosis of a VTE. Furthermore, the data suggest there is a lower risk of major bleeding with Rivaroxaban. Consequently, select patient groups can now be offered this treatment option. However, some unanswered questions will need to be addressed before Rivaroxiban completely replaces the older anticoagulants.
The optimal duration of anticoagulation with Rivaroxaban remains unknown. In patients with a first episode of a VTE, current CHEST guidelines (2) recommend anticoagulation of 3 months duration if a reversible cause is attributed to the pulmonary embolism. If there is no obvious cause, the patient should be continued on AC treatment for at least a 3-month period. Beyond this period, the guidelines advocate for a discussion between the patient and the physician in terms of risks of a re-occurrence versus those of bleeding associated with anticoagulant therapy. In case of a recurrent event, long-term anticoagulation is recommended. Certainly, given the ease of administration and dosing of Rivaroxiban, this treatment is an attractive substitute for a vitamin K antagonist. However, this current study only provides safety data for duration up to 12 months. Further studies are necessary to explore the optimal duration and long-term safety for anticoagulation with this drug. Whether the CHEST guidelines can be generalized to include the new oral anticoagulants remains to be seen.
Meanwhile, for patients with a cancer-related VTE, anticoagulation with LMWH remains standard of care. Dalteparin has a lower rate of recurrence compared to warfarin is this patient cohort (7). In this setting, the effectiveness of Rivaroxiban has not been sufficiently studied and consequently, it should not be substituted for LMWH. Similarly, there is no safety data of Rivaroxaban use in pregnancy, and as a result, LMWH remains the treatment of choice in this population. Finally, for patients with limited financial resources, Warfarin offers an inexpensive and equally effective treatment option compared to Rivaroxaban. Provincial funding for this drug is currently under review.
Rivaroxaban is the first oral anti-Xa inhbitor to be approved by Health Canada for the treatment of VTE. It provides a convenient and effective therapy for select patients as a substitute for Warfarin. As with any new drug, many unanswered questions remain. I am optimistic that we are standing at the brink of a new era of anticoagulation management.

References (Note: Article requests might require a login ID with CPSBC or UBC)

1. Rosamond W, Flegal K, Fridaz G, et al. Heart disease and stroke statistics – 2007 update: a report from the American Heart Association Statistics Committee ad Stroke Statistics Subcommittee. Circulation 2007; 115:e69-171 (View article)
2. Kearon C, Akl EA, Comerota AJ, et al; American College of Chest Physicians. Antithrombotic therapy for VTE disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(2):e419S-94S (View article with CPSBC or UBC)
3. Roehrig S, Straub A, Pohlmann J, et al. Discovery of the novel antithrombotic agent 5-chloro-N-({(5S)-2-oxo-3- [4-(3-oxomorpholin-4-yl)phenyl]-1,3-oxazolidin-5-yl}methyl)thiophene- 2-carboxamide (BAY 59-7939): an oral, direct factor Xa inhibitor. J Med Chem. 2005 Sep 22;48(19):5900-8 (View article with CPSBC or UBC)
4. Kubitza D, Becka M, Voith B, et al. Safety, pharmacodynamics and pharmacokinetics of single doses of BAZ 59-7939, an oral, director Factor Xa inhibitor. Clin Pharmacol Ther 2005;78:412-21 (View article with CPSBC or UBC)
5. Kubitza D, Becka M, Wensing G, et al. Safety pharmacodynamics and pharmacokinetics of BAY 59-7939 – an oral, director Factor Xa inhibitor – after multiple dosing in healthy male subjects. Eur J Clin Pharmacol 2005;61:873-80 (View article with CPSBC or UBC)
6. Büller HR, Prins MH, Lensin AW, et al. Oral Rivaroxaban for the treatment of symptomatic pulmonary embolism. N Engl J Med. 2012;366(14):1287-97 (View article)
7. Lee AY, Levine MN, Baker RI, et al. Low-molecular-weight heparin versus a coumadin for the prevention of recurrent venous thromboembolism in patients with cancer. N Engl J Med. 2003;349(2):146-53 (View article)

What is the issue

Burden of rotavirus: Rotavirus causes up to 40% of childhood gastroenteritis; virtually all children will have at least one episode by age 5, with at least 1 in 20 visiting the emergency department.  IMPACT has demonstrated that we have at least 450 cases per year of rotavirus leading to hospitalization in Canadian children’s hospitals. In addition to these hospitalizations, there is considerable burden on families and outpatient physician visits.  Worldwide, rotavirus is a major killer of children, causing up to 5% of deaths of children under the age of 5 years. Most severe rotavirus happens prior to the age of 2 years with the first episode; subsequent episodes are less likely to be severe.

A question I get asked frequently

Should I recommend the rotavirus vaccine & how safe is it? The rotavirus vaccine was funded as part of the public health care system in British Columbia in 2012.  There are two oral, live attenuated vaccines, Rotarix® (Glaxo-Smith-Kline) and Rotateq® (Merck).  Rotarix® has been chosen for the public health program in BC.  Questions that arise are (1) is it worth vaccinating against rotavirus? and (2) is it a safe vaccine – specifically, is it associated with intussusception like the Rotashield vaccine in the 1990s? Prior to 2012 in BC, uptake has been minimal.

Vaccine effectiveness & efficacy: In very large clinical trials, both vaccines were shown be highly efficacious at preventing severe rotavirus gastroenteritis, rotavirus-related emergency department visits and hospitalizations.  In 2007, with approximately half of American infants being vaccinated against rotavirus, surveillance in the United States showed a decrease of more than 50% of rotavirus diarrhea in all ages of children (not just those vaccinated).

Vaccine safety: Both rotavirus vaccine products have been shown to be safe and well tolerated.  A previous vaccine (Rotashield®, Wyeth) was linked to an excess risk of intussusception, so investigators, policy makers and physicians have been quite cautious.  With much larger than usual phase three Rotavirus vaccine trials and post-marketing surveillance, there has been no significant concern about excess cases of intussusception. While small numbers of Rotarix® vaccine trial participants (<5%) reported gastrointestinal upset, fever, or irritability, the proportion was the same in the placebo groups.  In the Rotateq® vaccine trials, there was a small, statistically significant increase in vomiting (15% vs. 14%) and diarrhea (24% vs. 21%).  The trials did not find any increased rates of severe adverse events.  Since both vaccines are live attenuated oral vaccines, there is some fecal excretion of the vaccine strain of rotavirus, but poses little danger to contacts (including immunocompromised contacts).

What I recommend (practice tip) to GPs in managing this problem?

The bulk of the evidence suggests that both rotavirus vaccines are safe and effective. They should be given as recommended by BCCDC at 2 and 4 months of age, with the other routine immunizations.  The information sheet for health practitioners (link added) suggests giving it at the beginning of a visit, while the child is happy. The vaccine is really sweet, so one could also give it around the time of the shots, as an adjunct pain relief. The first dose must be given between 6 and 20 weeks. The second dose must be given between 10 weeks and 8 months of age (minimum 1 month after dose 1).

Rotavirus vaccines can prevent important morbidity for young infants, and the associated physician visits, emergency department visits, hospitalizations and related parental stress and missed work days due to rotavirus infection.

References (Note: Article requests might require a login ID with CPSBC or UBC)

1. BC Centers for Disease Control. Section IIA – Immunization Schedules. Communicable Disease Control Immunization Program.  Available at http://www.bccdc.ca/dis-cond/comm-manual/CDManualChap2.htm
2. Immunize BC. Rotavirus Vaccine Program in British Columbia Information for Health Care Providers. February 2012. Available at http://immunizebc.ca/sites/default/files/graphics/hcp_qa_rotavirus_final-feb_9_2012.pdf
3. Le Saux N, Bettinger JA, Halperin SA, Vaudry W, Scheifele DW; for Members of the Canadian Immunization Monitoring Program, Active (IMPACT). Substantial morbidity for hospitalized children with community-acquired rotavirus infections. 2005-2007 IMPACT surveillance in Canadian hospitals. Pediatr Infect Dis J. 2010 Sep;29(9):879-82. (View article with CPSBC or UBC)
4. Le Saux N, Bettinger J, Déry P, Embree J, Vaudry W, Halperin SA, McDermid A, Booth TF, Coyle D. The hidden costs and characteristics of childhood rotavirus emergency visits in Canada. Pediatr Infect Dis J. 2012 Feb;31(2):159-63. (View article with CPSBC or UBC)
5. National Advisory Committee on Immunization (NACI).  Updated Statement on the use of Rotavirus Vaccines. Canada Communicable Disease Report  2010 Jul;36 (ACS-4). (View article)
6. Salvadori M, Le Saux N, Canadian Paediatric Society, Infectious Diseases and Immunization Committee. Recommendations for the use of rotavirus vaccines in infants. Paediatr Child Health. 2010;15(8):519-523 (View article)

What I did before

Atopic dermatitis (AD) is a chronic relapsing disease which involves pruritus and eczematous lesions, affecting 15% to 20% of the childhood population (1). Staphylococcus aureus infection is the most common complication of AD.
Patients with AD have a very high rate of S aureus colonization (76-100%) as compared to healthy controls (2-25%) (2, 3). Even when the S aureus is not causing a bacterial superinfection, its presence can exacerbate AD through superantigens which induce the release of proinflammatory cytokines.
While S aureus can be treated with topical and/or systemic antibiotics, it is preferable to avoid frequent antibiotic use on patients, especially with the emergence of community-acquired methicillin-resistant S aureus (CA-MRSA).

What changed my practice

In 2009, Huang et al published a study looking at whether or not suppression of S aureus growth with sodium hypochlorite (bleach) baths and intranasal mupirocin improves AD severity (4). In this study, they took 31 patients (aged 6 months to 17 years) with moderate to severe AD and evidence of bacterial infection and randomized them to receive active treatment versus placebo (they did not do bleach-only or no mupirocin group). After treating all with a 2 week course of cephalexin, participants were instructed to add 1/2 cup (0.12 L) of 6% bleach (treatment group) or water (placebo group) to a full bath of water and to bathe in this solution twice weekly for 3 months. Participants were also asked to apply mupirocin ointment (treatment group) or petroleum ointment (placebo group) intranasally for 5 consecutive days, once per month for 3 months.
After 3 months, the treatment group had a dramatic difference in their Eczema Area and Severity Index (EASI) score compared with placebo. As well, participants in the treatment group also showed a greater mean reduction in the proportion of BSA (body surface area) affected at both 1 and 3 month. Interestingly, these differences were only seen in the submerged areas, and not in the head and neck areas.

What I do now

Although the hallmark of AD treatment is education, avoidance of triggers, moisturization and topical anti-inflammatory medications (topical corticosteroids or topical calcineurin inhibitors), dilute bleach baths are an effective adjuvant antiinfective treatment that can help decrease the number of local skin infections and reduce the need for systemic antibiotics for patients with AD with heavily colonized and/or superinfected skin. I usually recommend 1/2 cup of 6% bleach for 1/3 to 1/2 of an adult bathtub. Earlier studies looking at the concentration needed to kill a resistant bacteria known as methicillin-resistant Staph aureus (MRSA) used higher concentrations (5). In general, I recommend to avoid getting this in the eyes and to use caution in those with a known allergy to bleach.  However, practically, there are no significant side-effects.  This concentration of dilute bleach is similar to what was used in the past to sterilize water.

References (Note: Article requests might require a login ID with CPSBC or UBC)

1. Eichenfield LF. Consensus guidelines in diagnosis and treatment of atopic dermatitis. Allergy. 2004;59(suppl 78):86–92 (View article with CPSBC or UBC)
2. Higaki S, Morohasi M, Yamagishi T, Hasegawa Y. Comparative study of staphylococci from the skin of atopic dermatitis patients and from healthy subjects. Int J Dermatol. 1999;38(4): 265–269 9. (View article with CPSBC or UBC)
3. Abeck D, Mempel M. Staphylococcus aureus colonization in atopic dermatitis and its therapeutic implications. Br J Dermatol. 1998;139(suppl 53):13–16. (View article with CPSBC or UBC)
4. Huang JT, Abrams M, Tlougan B, Rademaker A, Paller AS. Treatment of Staphylococcus aureus colonization in atopic dermatitis decreases disease severity. Pediatrics. 2009 May;123(5):e808-14. (View article with CPSBC or UBC)
5. Fisher RG, Chain RL, Hair PS, Cunnion KM.Hypochlorite killing of community-associated methicillin-resistant Staphylococcus aureus. Pediatr Infect Dis J. 2008 Oct;27(10):934-5 (Abstract, or view with CPSBC or UBC)

What I did before

If you have spent any time in the past year reading the BC College of Physicians and Surgeons’ quarterly newsletter, you are well aware that our governing body has significantly ramped up its Peer-Review Assessment Program.  This means more funding and training of assessors.  You would be well-advised then, particularly if you have been in practice for twenty years or more, to prepare for a visit from one of them sooner rather than later.

Oh, and one more thing.  When you do get the call, do not expect much sympathy from your family and friends that are not physicians.  I found that Joe Public LOVES the fact that doctors get a review of their practices once in a while!

What changed my practice

I underwent the assessment in the spring of 2011 and, like most practices, I discovered that there were some things I was doing well and some other things that could do with some improvement.  All in all though, I found the process neither punitive nor disciplinary in any way.  On the contrary, I was relieved that it was much more educational than I had expected.  My assessor was warm and helpful, and provided me with plenty of useful advice that I have since incorporated into my practice.

The assessment itself lasts about 4-5 hours and is broadly divided into three sections: the physical aspects and inner workings of the office, medical record-keeping, and the quality of care.

1. Physical Aspects and Inner Workings:  In this part of the assessment, the assessor reviewed my waiting room, examining rooms, emergency equipment, sterilizer, refrigerator, sample cupboard, chart storage area, sharps containers, opioid pads, and so on.  Of particular importance was maintaining patient privacy and confidentiality so fax reports, printers, telephone conversations, office charts, and other items of a potential delicate nature are inaccessible to snooping eyes and ears.The assessor also spent considerable time with my receptionist understanding how the flow of messages within the office functioned.  In other words, if my receptionist has a message for me, how does that message reach me?  And if I have a message for my receptionist, such as needing a chart pulled or wanting a patient to come in, how does that message reach her?  Several improvements in these inner workings were suggested in order to minimize the possibility of an action getting missed or something not being properly followed-up.
2. Medical Record Keeping:  The bulk of the peer-review assessment involved the examination of 15 patient charts.  First, the quality of the medical records was examined.  The gold standard here is a comprehensive SOAP-style note for each patient encounter.  In addition, however, the assessor also looked at my referral letters, pediatric growth charts, immunization records, pre-natal forms, and appropriate charting for all those GPSC initiatives (14050, 14051, 14033, etc.).  Of particular importance was having a proper at-a-glance summary sheet at the front of every chart, displaying chronic illnesses, previous surgeries, medications, allergies, family history, personal/social history, and so on.
3. Quality of Care:  Finally, the actual clinical management of the 15 selected patients was examined.  For patients with a chronic illness, was I following the recommended treatment guidelines?  And conversely, for healthy patients, was I doing the appropriate disease screening tests such as pap smears, mammograms, stools for occult blood, etc.  The assessor gave me many useful suggestions here, again to minimize the possibility of a patient falling through the cracks.

What I do now

Since having my assessment, I now pay very close attention to two very important questions whenever I write a note in a chart.  First, is it possible to determine why the patient presented, what was found out, and what was done about it?  And second, is the treatment adequate, including follow-up care for both acute and chronic conditions?  If you can answer in the affirmative to both these questions, then you can be fairly sure you are doing a good job.

The College has a mandate to protect the public, and as such, we must expect to have a review of our practices just like other professionals.  But an assessment is not necessarily a bad thing.  In fact, it may save you from an even worse fate one day!  Most civil actions initiated by patients, or patient complaints to the College, are due to either: a) poor communication, b) poor medical management, c) poor office organization such that something was missed, or d) misdiagnosis or a delay in diagnosis.  Making improvements in your office may preclude these things from happening or, if they do, will certainly put you in a much better position to defend yourself.  The peer-review assessment, as I look back on it now, mitigates risk.

This is borne out in the latest College newsletter:

1. “When a physician is the subject of a patient complaint, civil action, practice review, or billing audit, conclusions as to whether the care provided was acceptable inevitably turn to what has been documented in the clinical record…  A physician’s note is regarded as his/her intellectual footprint.”
2. “This College’s revalidation program regards the quality of recorded care as being a reasonable surrogate marker of competent medical care.”

So when the College does come calling, and they surely will, do not fear the worst.  Instead, think of the process as part of your life-long commitment to serving your patients as best you can.

Additional information

MPAC (Medical Practice Assessment Committee) https://www.cpsbc.ca/about-college/mpac and https://www.cpsbc.ca/about-college/practice-assessment.

September College Quarterly https://www.cpsbc.ca/files/u6/CQ_September_2012_Web.pdf page 8.

Participating physicians are eligible for MainPro C credits.

What I did before

I used to dread the frail old lady with dizziness – the history and examination was time consuming with vague findings in both, leading to uncertainty about diagnosis and cause. Worse, the medications we used helped little and falls were common.

My fears were compounded by research findings about the rising mortality and morbidity from falls, (1) which gave rise to the establishment of falls clinics – a wonderful idea but with long wait lists. Polypharmacy was clearly adding to the risks. Vertigo was particularly frustrating – easy to suppress the symptoms, but did this really help?

What changed my practice

About ten years ago, the earliest recommendations about the use of therapeutic manipulation of the head and repositioning of otoliths started to appear. Apart from some of the traditional skepticism that meets many manipulation therapies, the paper descriptions of the necessary steps appeared perplexing, problematic and painful to perform. “Rotating the neck 270°… ” seemed guaranteed to break something, including my confidence.

YouTube brought a variety of short clinical videos, demonstrating in more cogent form how to perform the Dix-Hallpike and Epley’s maneuvers, but the success rate remained low. The minor obstacle of finding a good teaching source also contributed to the low attempt rate. Then I discovered the DizzyFix app for the iPhone. Designed in Ottawa, this makes great use of the motion sensing in these devices. Be warned that it also acts as part-infomercial for other products from that company but this does not detract from the app’s usefulness.

You place your phone on the patient’s forehead. DizzyFix’s diagrams (2) walk you through the steps needed for the Dix-Hallpike and Epley’s maneuvers, including a real-time display of exactly what path and angle to move the patient’s head through, and a timer to introduce appropriate pauses. Patience and predictable positioning pay off!

DizzyFix App screen shots

What I do now

Because of simplicity of use and ready availability, I now use this app and promote its use amongst my colleagues and learners at our teaching clinic. The simple, self-explanatory steps with embedded tutorials reduce the time required to learn and teach so my colleagues are more apt (apped?) to use the maneuvers.

Now I can hear you say that not all dizziness is Benign Positional Vertigo. (3) Indeed the Falls Clinics emphasize the multifactorial nature of dizziness and a careful assessment of all cases. There is some helpful information included with DizzyFix. To address this need, I created a virtual patient case (4) to assist   colleagues and learners in thinking through such problems. The case provides more context and illustrates some of the common pitfalls in history, examination and management.

DizzyFix is available in the iPhone App Store but is not free. At present, there is no Android version available. In recommending this app, I have no conflict of interest.

References and further reading

1. Rogers C. Presbyastasis: A multifactorial cause of balance problems in the elderly. South African Family Practice 2010, May;52(5):431-4. (View)

2. DizzyFix iPhone Instruction Video. http://www.youtube.com/watch?v=Fk1hgJXzjQU

3. Labuguen RH. Initial evaluation of vertigo. Am Fam Physician. 2006;73:244-251 (View)

4. Topps. A dizzy blonde. Sharcfm virtual patient series: Available from: http://fmsharc.cfpc.ca/openlabyrinth/mstartnode.asp?mapid=82.

What care gaps I noticed

Depression can have devastating effects on the elderly and their families. Moreover, it is often under recognized, as it can present atypically, with agitation/ anxiety, somatic symptoms, or cognitive and functional decline rather than sadness and withdrawal. (1) It has been demonstrated to be associated with increased morbidity, mortality, and decreased quality of life. (2, 3)  It can cause severe hardship for caregivers because of behavioural issues and lead to premature institutionalization.

What data should be considered

By DSM IV definition (The 4th edition of “Diagnostic and Statistical Manual of Mental Disorders”), a major depression consists of depressed mood and lack of interest (anhedonia), plus four or more of the following: feelings of worthlessness or guilt, decreased concentration or ability to make decisions, decreased energy, psychomotor retardation or agitation, sleep or appetite disturbance, and preoccupation with thoughts of death, lasting more than 2 weeks.

The elderly can present atypically, often emphatically denying that they feel depressed. Instead, they may experience significant somatic symptoms, anxiety or irritability, delusional thinking involving unreasonable guilt, anxiety or fear, and marked executive impairment. This is common in patients suffering from acute (MI, CVA, hip fracture) and chronic (diabetes, osteoarthritis, incontinence, dementia) illnesses. Late onset alcohol or substance misuse may also mask an underlying depression.

What I recommend (practice tip)

Differential diagnosis

Frontotemporal dementias or apathetic delirium can masquerade as a depression, as can   drugs with CNS side effects, such as sedative/anxiolytics, alcohol, steroids, antihypertensives, or any drug with anticholinergic properties. Physical illnesses such as occult malignancies, chronic infections, endocrine abnormalities (hypo- or hyperthyroidism, hyperparathyroidism, diabetes), renal or hepatic impairment, anemia, Vitamin B12 deficiency, or multiple or frontal lobe strokes can also present as a depression.

History should include collateral information from a close friend or family member, a medication review and functional assessment*¹. As well as a physical exam, cognitive screening*² should also be done*³. Bloodwork could include a TSH, Vitamin B12, CBC, electrolytes, BUN, creatinine, and calcium. CT scan may be indicated by history or physical findings, to rule out frontal lobe pathology.

Antidepressants are likely no more effective than placebo in mild depression, (4) but are better than placebo for patients suffering from moderate to severe depressions. (5) All antidepressants are likely equally efficacious, but their side effect profiles differ. (6) They are likely no less effective in treating the elderly than younger patients, but reaching therapeutic dosage may be difficult because of other co-morbidities. For the elderly, a longer duration of therapy or switching regimens because of tolerability may be necessary.

Start low, go slow, and warn about potential side effects. Monitor medication compliance, and suicidal ideation. Consider limiting drug availability, especially if the patient is confused, or there is a risk of suicide. Tricyclic antidepressants are to be avoided because of side effects. Treat for 9-12 months after finding an effective drug, perhaps indefinitely if this episode represents a recurrent or severe depression. Abrupt withdrawal of an SSRI can lead to increased anxiety, irritability, dizziness and nausea.

Treatment options include serotonin reuptake inhibitors, such as citalopram, 20-30 mg/day, or escitalopram, 10-20 mg/day. Main side effects include hyponatremia, anxiety, insomnia, GI upset, and QT prolongation. The serotonin-noradrenergic reuptake inhibitor venlafaxine 75-225 mg/day in divided doses can cause the same side effects as the SSRI’s as well as hypertension, tachycardia and urinary retention. Mirtazapine 15-30 mg at hs can be useful for treating symptoms of insomnia and anxiety, and can also lead to weight gain.

It is important to recommend non-pharmacologic treatment modalities such as homemakers, nutritional assistance or supplements, exercise, caregiver support and counselling, and possibly a move to housing with increased assistance.

Cognitive Behavioural Therapy appears to be more effective than “usual care” in elderly patients with mild to moderate depression, but does not seem to add to the effectiveness of antidepressant therapy. (7)

Electroconvulsive therapy may be necessary for patients who are too fragile to wait the 2-3 months it may take for antidepressants to work, or are unable to tolerate the side effects. It should also be considered for those who are psychotically depressed, and for those for whom ECT was effective in the past. ECT can be done as an outpatient, but most frail elderly require hospitalization. If you feel that your patient may be a candidate, a Psychiatry referral is necessary, usually through the local Older Adult Mental Health Team. A Geriatric Psychiatrist may be more comfortable giving ECT to a frail, medically complex patient.

The benefits of using a neuroleptic along with an antidepressant in elderly patients likely do not outweigh the risks – (extrapyramidal side effects, excess cardiovascular death). It is better to augment therapy with another antidepressant, such as buproprion, or switch agents if not effective.

Patients should be referred to a Psychiatrist if the diagnosis is in question, the depression seems refractory to treatment, or the patient is at risk to harm themselves or others.

*1.  Functional screening: The formal scales most commonly used is the Katz index of Activities of Daily Living Scale, and the Lawson Index of Instrumental Activities of Daily Living Scale. Dr. John Sloan, a family physician with special interest in care of the elderly has popularized “DEATH” (dressing, eating, ambulating, toileting and hygiene) and “SHAFT” (shopping, housework, accounting, food preparation and transportation). I would add “ability to manage medications” under the “a”. I will usually ask whether or not the patient has difficulty with bathing, as it is the most difficult ADL. If there are difficulties, I will ask about the other ADL’s. I will also ask if there is anyone assisting them with house hold chores. Collateral information is  important to verify what is reported by the patient, as they may forget, confabulate, or deliberately exaggerate their capabilities out of embarrassment, or for fear of consequences.

*2. Cognitive Screening: the Folstein Minimental Status exam and the Montreal Cognitive Assessment exam are quick, easily reproducible screens for cognitive impairment. The MOCA is more useful for detecting Minimal Cognitive Impairment, or problems with frontal/executive function. Another quick screen is the clock drawing test (you get the patient to draw a clock, putting the numbers on correctly, and putting the hands of the clock to say “10 after 11”).

*3. Screening for depression can be done easily with the Geriatric Depression Scale, Short Form, which includes 15 yes or no questions. A score of greater than 5 points is suggestive of a major depression. The Patient Health Questionnaire-9 (PHQ 9) is also a self administered questionnaire that can be used to screen for depression. Both are quick to do in an office setting, and appear to be equivalent as screening tools. (8)

References (Note: Article requests might require a login ID with CPSBC or UBC)

1  Blazer DG Depression in Late Life: Review and Commentary Journal of Gerontology: J Gerontol A Biol Sci Med Sci 2003; Vol 58A, no 3 249-265 (View article with CPSBC or UBC)

2.  Hoen PW et al. Differential associations between specific depressive symptoms and cardiovascular prognosis in patients with stable coronary heart disease. J Am Coll Cardiol Sept 7 2010; 56: 838 (View article, or view with UBC)

3.  Rovner BW Depression and increased risk of mortality in the nursing home patient. Am J Med May 1993 94 (5A) 19S-22S (View article with CPSBC or UBC)

4. Turner EH – Selective publication of antidepressant trials and its influence on apparent efficacy NEJM Jan17 2008; 358(3): 252-60 (View article with CPSBC or UBC)

5. Fournier JC Antidepressant drug effect and depression severity: a patient level meta-analysis JAMA Jan 6 2010; 303 (1) : 47-53 (View article)

6. Sinyor M The Sequenced Treatment Alternative to Relieve Depression (STAR-D) trial: a review Can J Psych March 2010; 55(3) : 125-35 (View article with CPSBC or UBC)

7. Cognitive and Behavioural Therapy and Reminiscence techniques for treatment of depression: a systematic review. Peng XD; J Int Med Res July 1/09 37(4): 975-82 (View article with CPSBC or UBC)

8. A study of diagnostic accuracy of the PHQ-9 in primary care elderly. Phelan E BMC Fam Prac Jan 1/10; 11:63 (View article with CPSBC or UBC)

What I did before

The Framingham Study (which started in 1948) introduced the term “risk factors for cardiovascular disease” [1, 2]. Ever since, most physicians including myself have used the Framingham data and tables to assess the patients’ risk [3, 4]. This resulted in a remarkable decline in cardiovascular disease – it is no more the leading cause of death in Canada.   While most of the risk factors can be identified by doing personal and family history of cardiovascular disease (CVD) laboratory data had been used by Framingham and other risk scoring algorithms.

Thus, most of us concentrated on lipid profile, especially LDL-cholesterol which became the focus of treatment [4].  Additional risk factors have also been identified including lipoprotein(a) which is particularly important to measure in individuals with strongly positive family history of CVD and a number of other less important biomarkers [5, 6, 7].

What changed my practice

In 2001, I started collaborating with a Montreal cardiologist, Dr. Allan Sniderman who has been an advocate for using apolipoprotein B for risk assessment [8].  His rationale was that, as there is one molecule of apo B per each LDL particle and the LDL half-life in plasma is much longer than that of the other apo B containing lipoproteins, the concentration of apo B reflects the LDL particle number in plasma. A patient who has, for example, an LDL-cholesterol level of 3.0 mmol/L may have an apo B which is low (say 0.8 g/L if this LDL-cholesterol is carried on large LDL particles) or apo B of 1.6 or higher (if the cholesterol is carried on small dense LDL particles). In addition, several studies established that apo B is a better predictor of risk both at baseline and on treatment than LDL-C [9, 10, 11]. This is due to the fact that small dense LDL particles are much more atherogenic as they easily penetrate the endothelial space.

In patients with triglyceride over 4.5 mmol/L, LDL-C cannot be calculated and thus the measurement of apo B is of additional advantage.  Moreover, numerous studies have shown that LDL-cholesterol goal does not always mean that apo B treatment target has been achieved [12].  Apo B has been shown to be a better predictor of outcomes on treatment, especially in patients with hypertriglyceridemia, such as individuals with diabetes or metabolic syndrome.  The other advantage is that apo B can be measured on a non-fasting specimen.

What I do now

Ideally, I try to obtain with the initial lipid profile also the concentration of patients’ apo B.  This is important for two reasons: first, in patients with hypertriglyceridemia the apo B will help me to differentiate between familial combined hyperlipidemia (these patients have high apo B) and familial hypertriglyceridemia (these patients have normal or low apo B).  After starting treatment in patients where the major problem is hypercholesterolemia, the follow up lab test may be apo B alone.  Again, the advantage here is that it can be done on a non-fasting specimen and is less expensive than repeating the whole lipid profile.

However, two recent papers (both “metaalanyses”) question the superiority of apo B measurement [13, 14].  In the first, the authors suggest that use of non-HDL-cholesterol (total cholesterol-HDL cholesterol) is preferable, although the differences from the results of apo B are only marginal [13].  In the second metaanalysis the authors claim no advantage in measuring of apolipoproteins [14].  Both papers are open to a number of criticism and contradict the results of several previous studies and one contrary metaanalysis in favor of apo B [15].  Thus, the Canadian guidelines continue to recommend the use of apo B as a treatment target [4].

References (Note: Article requests might require a login ID with CPSBC or UBC)

1. Thomas R. Dawber, Gilcin F. Meadors, and Felix E. Moore, Jr. Epidemiological Approaches to Heart Disease: The Framingham Study. Am J Public Health Nations Health. 1951; 41: 279–286. (View article with CPSBC or UBC)
2. Dawber, Thomas R., and Moore, Felix E. (1952), “Longitudinal Study of Heart Disease in Framingham, Massachusetts: An Interim Report,” in Research in Public Health, Papers presented at the 1951 Annual Conference of the Milbank Memorial Fund, 241-247. (View article with CPSBC)
3. O’Donnell CJ, Elosua R.  Cardiovascular risk factors. Insights from Framingham Heart Study. Rev Esp Cardiol. 2008; 61:299-310 (View article with CPSBC or UBC)
4. Genest J, McPherson R, Frohlich J et al. 2009 Canadian Cardiovascular Society/Canadian guidelines for the diagnosis and treatment of dyslipidemia and prevention of cardiovascular disease in the adult- 2009 recommendations. Can J Cardiol 2009; 25: 567-579. (View article)
5. Bostom AG, Gagnon DR, Cupples LA, et al. A prospective investigation of elevated lipoprotein (a) detected by electrophoresis and cardiovascular disease in women. The Framingham Heart Study.Circulation 1994; 90:1688-95. (View article with CPSBC or UBC)
6. Ridker PM, Hennekens CH, Stampfer MJ. A prospective study of lipoprotein(a) and the risk of myocardial infarction. JAMA 1993; 270:2195-9. (View article with CPSBC or UBC)
7. Danesh J, Collins R, Peto R. Lipoprotein(a) and coronary heart disease. Meta-analysis of prospective studies. Circulation 2000; 102:1082-5. (View article with CPSBC or UBC)
8. Sniderman AD, Bergeron J, Frohlich J. Apolipoprotein B versus lipoprotein lipids: vital lessons from the AFCAPS/TexCAPS trial. CMAJ. 2001; 164:44-7. (View article)
9. Lamarche B, Tchernof A, Moorjani S, et al. Small, dense low-density lipoprotein particles as a predictor of the risk of ischemic heart disease in men. Prospective results from the Quebec Cardiovascular Study. Circulation. 1997; 95:69–75. (View article with CPSBC or UBC)
10. Lamarche B, Moorjani S, Lupien PJ, et al. Apolipoprotein A-I and B levels and the risk of ischemic heart disease during a five-year follow-up of men in the Quebec cardiovascular study. Circulation. 1996; 94:273–8 (View article with CPSBC or UBC)
11. Gotto AM Jr, Whitney E, Stein EA, Shapiro DR, Clearfield M, Weis S, Jou JY, Langendörfer A, Beere PA, Watson DJ, Downs JR, de Cani JS. Relation between baseline and on-treatment lipid parameters and first acute major coronary events in the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS). Circulation. 2000; 101:477-84. (View article with CPSBC or UBC)
12. Idris I, Tate H, Ahmad A, McCormack T. Concordance between plasma apolipoprotein B levels and cholesterol indices among patients receiving statins and nonstatin treatment: Post-hoc analyses from the UK. InPractice study. J Clin Lipidol. 2011; 5:316-23. (View article with CPSBC or UBC)
13. Boekholdt S. M, Arsenault B, Mora S, Pedersen T, et al. Association of LDL Cholesterol, Non–HDL Cholesterol, and Apolipoprotein B Levels With Risk of Cardiovascular Events Among Patients Treated With Statins.Meta-analysis. JAMA. 2012; 307:1302-09. (View article with CPSBC or UBC)
14. The Emerging Risk Factors Collaboration, Di Angelantonio E, Gao P, et al. Lipid-Related Markers and Cardiovascular Disease Prediction. JAMA. 2012; 307:2499-506. (View article with CPSBC)
15. Sniderman AD, Williams K, Contois JH, et al. A meta-analysis of low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein B as markers of cardiovascular risk. Circ Cardiovasc Qual Outcomes. 2011; 4:337-45. (View article with CPSBC or UBC)

What I used to do

In family practice, I only occasionally recommended an HIV test outside of antenatal care. At the sexual health clinic, I encouraged ‘higher risk’ patients to get tested. But I did not routinely offer and recommend an HIV test to all adults, in either of my practices.

What changed my practice

Routine HIV testing for all adults is now recommended^1,2  by Vancouver Coastal Health, Providence Health and the BC Centre for Excellence in HIV/AIDS. The United States³, United Kingdom⁴, France⁵ and the World Health Organization⁶ are among those preceding Canada with guidelines for expanded HIV testing. Specifics of those recommendations vary, but the goal is the same: to reduce the proportion of individuals with HIV infection who remain undiagnosed or present late for care.

It’s estimated that 1/4 of Canadians living with HIV are unaware that they are infected⁷. That translates to about 3,500 people in British Columbia^2,8 who may unknowingly infect others with the virus, and who may benefit from treatment if diagnosed. In BC, about 65% of diagnoses occur after our patients should already be on treatment⁹, with up to 17% having advanced disease at the time of diagnosis¹⁰.

Rationale for routine HIV testing is summarized here in a few key points:

Treatment works

Highly active antiretroviral therapy (HAART) has changed HIV from death sentence to manageable chronic disease. People treated early can live long and productive lives, with lifespans approaching that of the general population¹¹. BC’s HIV treatment guidelines recommend beginning antiretroviral (ARV) therapy earlier in the course of infection – at CD4 count of 500 cells/mm³, sometimes higher¹². ARV medication is free in this province.

Treatment as prevention

HIV/AIDS researchers debated whether ARV treatment that effectively suppresses viral replication might also reduce transmission rates¹³. Then, the HIV Prevention Trials Network (HPTN) announced in May 2011 that the 052 clinical trial had demonstrated a 96% reduction in heterosexual HIV transmission¹⁴.  “Because of HPTN 052’s profound implications for the future response to the AIDS epidemic”¹⁵, the journal Science chose it as 2011 Breakthrough of the Year.

Risk-based testing has fundamental limitations

Consider the Vancouver Mancount study¹⁶ in a population with known risk: 20% of gay men had never told a healthcare provider that they had sex with men; only 51 % had been tested for HIV in the previous year; and 23% of the under 30 years olds had never been tested. Improving how, when and who we ask about risk is clearly necessary; but it’s not sufficient. Up to 1/4 of people testing positive report no risk factors¹⁷. And even if they know, and we ask, many people still will not disclose their risk behaviors to us.

Expanded testing is cost effective

Evidence supports expanded HIV testing even when the HIV prevalence is as low as 0.5-2 cases per 1000¹⁸. Estimates¹⁹ put Vancouver at 12/1000 diagnosed prevalence, and BC at 2.2/1000. Vancouver may skew BC’s rate estimate, but keep in mind that diagnosed prevalence is tied to testing activity. Therefore, a recommended approach is to begin routine testing and to reassess if no new cases are found after a large number of tests – e.g. if no new cases are identified after 4000 patients are tested, 95% CI for a prevalence of < 0.1% would have been achieved¹⁸. I would expect that Public Health will advise us when to stop, but they won’t have the data to do so until we actually start.

By the way, Vancouver’s acute care pilot project, where patients are offered HIV testing upon admission to hospital, has to date resulted in a new diagnosis rate of 10 per 1000²⁰ – not only cost-effective, but a rate that may be cost-saving²¹.

Missed opportunities for timely diagnosis under the old testing paradigm

In the Vancouver acute care pilot²⁰ there have been 18 new diagnoses to date. Half have had CD4 counts of < 200 cells/mm³. Consistent with published research²², many have had multiple encounters with the healthcare system – including family physicians – prior to their diagnosis by consensual routine testing in hospital. These patients are ethnically diverse, one third are > 50 yrs old and most are male. The vast majority of patients offered a test accept^20,23, but a much smaller proportion of eligible patients are offered one²⁰.

Imagine if we all adopted a practice of routine HIV testing in both acute and community care – or even just began by ordering a couple more tests per day. We might alter the course of HIV for one of our patients… or perhaps for all of BC.

What I do now

I offer and recommend an HIV test to any adult who has not been tested in the past year:

• whenever other bloodwork is ordered;
• whenever I test for or diagnose a Sexually Transmitted Infection (STI), Hepatitis C or Tuberculosis²; and
• whenever I’m asked for an HIV test.

For patients with identified risk I recommend more frequent testing, e.g. every 3-6 months²⁴. I continue to routinely recommend HIV testing with prenatal bloodwork.

I also:

• Make testing routine: “It is now recommended, and so I ask everyone…”.  Normalizing language is destigmatizing, and routinizing the offer also helps me to remember. The majority of patients accept an HIV test when offered one^20,23.
• Obtain verbal consent: “May I add an HIV test to your lab work?”  As with all medical interventions, consent is required.
• Provide a print information handout²⁵ to complete the information part of consent. The handout at HealthLink BC ²⁶ is available in 6 languages.
• Chart as for any other tests.
• Manage negative results as for other tests.

Note that for most patients, extensive pre- and post-test counseling is no longer required²⁵. That said, benefit from more discussion with my higher risk patients is expected – no different from other conditions where one assesses pre-test probability of a positive test to be high, or ongoing risk is known.

And when I lapse from the routine, I remind myself of my last HIV diagnosis –  a woman in her early 20s. She came in for a PAP, and STI screening was offered because she hadn’t had that since getting together with her current partner. HIV testing was also recommended. Last I heard, she and her partner were both on ARVs and getting on with their lives.

Resources:

• Expanded HIV testing guidelines will improve early diagnosis. STOP HIV/AIDS Update No.3 Spring/Summer 2011 – page 3, for a succinct statement on new HIV testing recommendations. (View)
• Qaseem A, et al. Screening for HIV in health care settings: a guidance statement from the American College of Physicians and HIV Medicine Association. Ann Intern Med. 2009;150:125-131 -  a good critical review of US Guidelines- (View with CPSBC). Or in brief: Graham L. ACP releases guidance statement on screening for HIV. Am Fam Physician. 2009;80:405-407. (View)
• Gilbert M, Krajden M. Don’t wait to test for HIV. BCMJ 2010;26:308 – B.C. specific information on testing frequency and window periods. (View)
• CTV News: Interview with Dr. Patricia Daly, Chief Medical Health Officer for Vancouver (View)
• Patient Handout from Health Link BC: HIV and HIV Tests – available in English, Chinese, French, Punjabi, Spanish, Vietnamese. (View)
• Physician Frequently Asked Questions (View)
• It’s Different Now is an award winning social media campaign that may lead your patients to ask you about HIV testing (View)
• Visit hiv.ubccpd.ca for more information and resources

STOP HIV/AIDS* and UBC Division of Continuing Professional Development have partnered to offer a range of educational opportunities about HIV testing, based on what physicians have told us is important. Visit http://hiv.ubccpd.ca for more information; for resources to help you with implementation of routine HIV testing in your practice; and to register for accredited educational offerings – including Webinars, Interactive Workshops, In-practice Support, and Linking Learning to Practice.

* Seek and Treat to Optimally Prevent (STOP) HIV/AIDS is a provincially funded project within Vancouver Coastal Health, Providence Health, Centre for Excellence in HIV & AIDS, and Northern Health – aimed at improving HIV care along the complete continuum, from detection through access and delivery. The HIV Testing Initiative in Family Practice is just one among Vancouver Coastal Health’s STOP HIV/AIDS projects. UBC Division of Continuing Professional Development is leading this initiative for Vancouver’s family physicians, with the aim of increasing HIV testing through physician engagement in quality educational programming.

References: (Note: Article requests require a login ID)

1. Gustafson R, Steinberg M. Expanding provider-initiated HIV testing. BCMJ 2011;1: 13,49. (View)
2. STOP HIV/AIDS Update No.3 Spring/Summer 2011. (View)
3. Centers for Disease Control and Prevention. Revised recommendations for HIV testing of adults, adolescents, and pregnant women in health-care settings. MMWR 2006;55(No. RR-14). (View)
4. British HIV Association, British Association for Sexual Health and HIV, British Infection Society. UK national guidelines for HIV testing. September, 2008. (View)
5. Haute Autorité de Santé. HIV infection screening in France: Screening Strategies. Executive Summary and Guidelines. October 2009. (View)
6. World Health Organization. Guidance on couples HIV testing and counselling including antiretroviral therapy for treatment and prevention in serodiscordant couples – recommendations for a public health approach. Switzerland: April 2012. (View)
7. Public Health Agency of Canada. Summary: Estimates of HIV Prevalence and Incidence in Canada, 2008. (View)
8. BC Centre for Disease Control in Annual Surveillance Report: HIV and Sexually Transmitted Infections, 2010.  Note: calculation is based on estimate of undiagnosed HIV 26%⁷ and Public Health Agency of Canada HIV prevalence estimate⁸. (View)
9. Gustafson R. (Medical Health Officer, Vancouver Coastal Health, Vancouver, BC). BC Public Health Surveillance Unit and British Columbia Centre for Excellence in HIV/AIDS Drug Treatment Program: Data linkage project, 2011. Communication with: MB Collins (Physician Lead, HIV Testing Initiative in Family Practice, S.T.O.P. HIV/AIDS project, Vancouver Coastal Health). 5 July 2012.
10. Rank C, et al. Advanced HIV disease at time of diagnosis in British Columbia,1995-2008.  BC Centre for Disease Control Special Report, 2011. (View)
11. May M, et al. Impact of late diagnosis and treatment on life expectancy in people with HIV-1: UK Collaborative HIV Cohort (UK CHIC) Study. BMJ 2011;343:d6016 doi: 10.1136/bmj.d6016 (View)
12. BC Centre for Excellence in HIV/AIDS Therapeutic Guidelines Committee. Antiretroviral Treatment (ARV) of adult HIV infection. 2011. (View)
13. Montaner JS, Hogg R, Wood E, et al. The case for expanding access to highly active antiretroviral therapy to curb the growth of the HIV epidemic. Lancet 2006;368:531-536. (View with CPSBC)
14. Cohen MS, et al. Prevention of HIV-1 Infection with Early Antiretroviral Therapy. N Engl J Med 2011;365:493-505. (View)
15. Cohen J. Breakthrough of the year – HIV treatment as Prevention. Science 2011;334:1628. doi:10.1126/science.334.6063.1628. (View with CPSBC)
16. Trussler T, et al. ManCount Sizes-up the Gaps: a sexual health survey of gay men in Vancouver. Vancouver Coastal Health: Vancouver, 2010. (View)
17. Chou R, et al. U.S. Preventive Services Task Force. Screening for HIV: a review of the evidence for the U.S. Preventive Services Task Force. Ann Intern Med. 2005;143:55-73. (View)
18. Qaseem A, et al. Screening for HIV in health care settings: a guidance statement from the American College of Physicians and HIV Medicine Association. Ann Intern Med. 2009;150:125-131. (View with CPSBC)
19. Gustafson R. (Medical Health Officer, Vancouver Coastal Health, Vancouver, BC). Vancouver: number of people known to BCCFE as being linked to care divided by Vancouver’s population; BC: BCCDC prevalence estimates divided by population above 15 years of age. Communication with: MB Collins (Physician Lead, HIV Testing Initiative in Family Practice, S.T.O.P. HIV/AIDS project, Vancouver Coastal Health). 22 June 2012.
20. Gustafson R. (Medical Health Officer, Vancouver Coastal Health, Vancouver, BC). Communication with: MB Collins (Physician Lead, HIV Testing Initiative in Family Practice, S.T.O.P. HIV/AIDS project, Vancouver Coastal Health). 5 July 2012.
21. Hutchinson AB, et al. Return on public health investment: CDC’s Expanded HIV Testing Initiative. J Acquir Immune Defic Syndr 2012;59:281-6. (View with CPSBC)
22. Sullivan AK, et al. Newly diagnosed HIV infections: review in UK and Ireland. BMJ 2005;330:1301-2. (View)
23. Health Protection Agency. Time to test for HIV: Expanding HIV testing in healthcare and community services in England. Final report, 2011. [accessed 1 July 2012] (View)
24. Gilbert M, Krajden M. Don’t wait to test for HIV. BCMJ 2010;26:308. (View)
25. BC Centre for Disease Control. Communicable Disease Control Manual Chapter 5 – Sexually Transmitted Infections, HIV Pre and Post Test Guidelines, September 2011. [accessed 15 June 2012] (View)
26. Health Link BC. HIV and HIV Tests. STI Series – Number 08m September 2011. Available in English, Chinese, French, Punjabi, Spanish, Vietnamese. [accessed 13 June 2012] (View)

What I did before

Travellers’ diarrhea (TD) is by far the most common cause of morbidity in persons travelling abroad.  Incidence rates range from 30-70%¹ on a 2-week vacation in a developing country, depending on the destination.  Unlike in Canada, where the majority of gastroenteritis is of viral etiology, the majority of diarrhea in a developing country is caused by bacterial pathogens; noteably E. Coli, Camplylobacter, Shigella and Salmonella, followed by viral and parasitic causes. The morbidity is significant in terms of time lost to leisure or business activities, and, although, most people recover spontaneously 3 to 5 days, some may have a considerably prolonged course.

After working in the field of Travel Medicine for nearly 20 years, I realize I spend a lot of time counselling travellers about recommended and required vaccines and malaria preventive medications.  Rarely do travellers encounter morbidity or mortality from these particular infectious diseases.  This caused me to evaluate the evidence for prevention of TD, to see if there was some advice that I could give in the pre-travel consult that would, indeed, improve the health of the majority of the travelling public.

My focus traditionally had been placed on food and water precautions, hand washing and food selection, along with some discussion around the use of bismuth subsalicylate² and probiotics in prevention of diarrhea, before entering into the larger discussion about oral rehydration, over the counter and antibiotic treatments for the same.³

What changed my practice

The approval of the oral whole cell cholera and traveller’s diarrhea vaccine (WC/rBS) (Dukoral™) in Canada in 2003 promised a novel approach to the prevention of TD.  Certainly the advertising was compelling!  This vaccine works by developing antibodies in the gut mucosa to cholera toxin.  The B-subunit of cholera toxin is immunologically similar to heat labile toxin produced by Enterotoxigenic E.coli (ETEC).  ETEC produces both heat labile and heat stable toxin.

In people who acquire TD in the developing world, approximately 50% is due to ETEC, of which 50% is heat labile toxin.  After ingestion of the WC/rBS vaccine, there is some short lived cross reactivity to the ETEC heat labile toxin that lasts about 3 months.  The efficacy of this vaccine is about 67% for ETEC.⁴’ ¹¹ This results in an overall theoretical absolute risk reduction of 0.5×0.5×0.67=16.75% for all cases of TD.

There are various ways to evaluate effectiveness of the vaccine:

1. In a study of Spanish travellers who presented to a travel clinic prior to their journey, the incidence of TD was 23% in people who took the WC/rBS vaccine, and 40% in those who had not, for all travel destinations visited.  This is equal to a 17% absolute risk reduction.  However, this can also be reported as a 43% relative risk reduction in occurrence of TD.⁵   Another way of looking at the data in this study concluded that the number needed to treat to prevent one traveller from suffering from an episode of TD was 5.8, which might seem worthwhile compared to many of our other medical interventions.  Statistics can say many things depending on how they are presented.
2. A study of Finnish tourists to Morocco showed a decrease in overall incidence of TD by 23% in those who had taken the WC/rBS vaccine.  Specifically, this study found the vaccine to be 52% protective against ETEC strains.  More interestingly, this study found this vaccine to have a protective efficacy of 71% against the combination of ETEC and any other bacterial pathogen.  The authors surmised that protection against one component of a mixed infection enables the immune system to defend more effectively against other pathogens. ⁶

A significant variable is that ETEC accounts for different proportions of TD in different countries and in different seasons, and this is continually changing with time.  Therefore the effectiveness of this vaccine varies considerably based on destination and type of travel, making it difficult to know how to interpret these studies when one is discussing the topic with the travelling public!

What I do now

In my practice, I always talk about this vaccine with persons travelling to less developed countries in conjunction with the other diarrhea preventive advice.  Other TD prevention strategies might give better protection against all-cause diarrhea illness, rather than targeting a specific organism.

I clarify that the use of this vaccine does not give the traveller free reign to safely indulge in risky type food ingestion.

I more strongly recommend it to certain populations who are more prone to TD, or who might be more at risk of serious consequences from TD.⁷   These include people on proton pump inhibitors with gastric hypochlorhydria, the young and the elderly, those with chronic illness, people with inflammatory bowel disease, the immune- compromised, and those who have a history of repeated severe TD. A recent analysis of the use of this vaccine for leisure travellers demonstrated that if the rates of ETEC caused TD in the country visited exceeded 13%, it would be a cost effective measure.  However, the ‘perceived value’ of the trip for an individual traveller ultimately decides if this vaccination provides good value for money.⁸

I do continue to discuss hand washing, food choice and water hygiene as preventive measure for TD with the travelling public, as these measures intuitively make sense, although, admittedly with less evidence base than I would have thought backing me up!⁹

References and additional reading: (Note: Article requests might require a login ID with the BC College of Physicians website or UBC)

1. Arguin P, Kozarsky P, Navin A., ed.  Health Information for International Travel. U.S. Department of Health and Human Services Centers for Disease Control and Prevention. 2012; Chapter 2, Travellers’ Diarrhea (View article)
2. DuPont, H et al. Prevention of Travellers’ Diarrhea by the Tablet Formulation of Bismuth Subsalicylate.  JAMA. 1987; 257:1347-50. (View article with CPSBC or UBC)
3. DuPont et al. Expert Review of the Evidence Base for Prevention of Travelers’ Diarrhea.  Journal of Travel Medicine 2009 May/June; 16(3):149-60. (View article with CPSBC or UBC)
4. Clemens, J.D., et al.  Field Trial of oral cholera vaccines in Bangladesh: results from three year follow up.  Lancet 1990;335(8684):270-73 (View article with CPSBC or UBC)
5. Lopez-Gigosos R. et al.  Effectiveness in prevention of Travellers’ Diarrhoea by an oral cholera vaccine WC/rBS.  Travel Med Infect Dis. 2007 Nov; 5(6):380-4. (View article with CPSBC or UBC)
6. Peltola H, Siitonen A, Kyronseppa H, et al. Prevention of Travellers’ Diarrhea by oral B-subunit/whole cell cholera vaccine.  Lancet 1991; 338(8778):1285-9. (View article with CPSBC or UBC)
7. Canadian Immunization Guide, 7^th edition.  Public Health Agency of Canada. 2006; 158-165 (View article)
8. Lundkvist, J., Steffen, R., et al. Cost-Benefit of WC/rBS Oral Cholera Vaccine for Vaccination Against ETEC-Caused Travelers’ Diarrhea.  Journal of Travel Medicine2009 Jan/Feb; 16(1):28-34 (View article with CPSBC or UBC)
9.  Kozicki M, Steffen R, Schar M. ‘Boil it, cook it, peel it or forget it’: does this rule prevent travellers’ diarrhea?  Int J Epidemiol 1985: 14:169-172. (View article with CPSBC or UBC)
10. Committee to Advise on Tropical Medicine and Travel (CATMAT).  Statement on travellers’ diarrhea.  Canada Communicable Disease Report 2001; 27(ACS3):1-12. (View article)
11. Committee to Advise on Tropical Medicine and Travel (CATMAT).  Statement on new oral cholera and travellers’ diarrhea vaccination.  Canada communicable Disease Report 2005; 31(ACS7):1-12. (View article)
12. BC Guidelines link to Infectious Diarrhea: http://www.bcguidelines.ca/guideline_diarrhea.html

What I did before

Children are less physically active than in previous generations. With advances in computer based gaming, safety concerns and sedentary life style of today’s families, children have been significantly less active. This resulted in higher rates of children fulfilling the criteria for ‘overweight’ and ‘obese’.

Children 8- 18 years old spend close to 25% of their awake time watching TV, resulting in increased rate of obesity [1]. With the use of more screen-based gaming and communication devices, the portion may be even higher.

Several studies in the past, both in a laboratory based investigation as well in real-life circumstances research, reported that children playing active video games have a moderate or vigorous levels of physical activity [2-4].

I used to recommend to families to engage their children in active video games if they decide to purchase a gaming system, in hopes that these games will enhance physical activity by moving and dancing in front of the screen.

What changed my practice

A recent study [5] by a group from the Baylor College of Medicine in Houston, Texas, suggests that active video games have no effect on the amount of physical activity in children, compared to non-active games. Eighty four children were recruited, and along with their parents completed surveys. They were randomized to receive two computer games that were either very active games or inactive games. The children wore accelerometers for 7 days in order to measure their physical activity levels.

There was no difference in level of physical activity between the groups. The authors suggested that children with the active games either did not do more activity or compensated for the increased intensity by being less active at other times in the day.

What I do now

There is no alternative to healthy outdoor physical activity. I now recommend to all parents (with overweight/obese children or not) to significantly limit use of video games and other screen-based devices for their children, and to remove them from the child’s room, if possible. While no clear recommendations exist, I suggest to parents to limit screen time to an hour a day during weekdays. Parents should support their child’s healthy living by following the Canadian Paediatric Society’s recommendation [6] to have 60-180 minutes a day (!) of physical activity in different intensities for all children.

References / Additional reading (Note: Article requests might require a login ID with CPSBC or UBC)

1. Robinson TN. Television viewing and childhood obesity. Pediatr Clin North Am. 2001;48(4):1017-25 (View article with CPSBC or UBC)

2 Bailey BW, McInnis K. Energy cost of exergaming: a comparison of the energy cost of 6 forms of exergaming. Arch Pediatr Adolesc Med. 2011;165(7):597–602 (View article with CPSBC or UBC)

3. Barnett A, Cerin E, Baranowski T. Active video games for youth: a systematic review. J Phys Act Health. 2011;8(5):724-737 (View article with UBC)

4 Madsen KA, Yen S, Wlasiuk L, Newman TB, Lustig R. Feasibility of a dance videogame to promote weight loss among overweight children and adolescents. Arch Pediatr Adolesc Med. 2007;161(1):105–107 (View article with CPSBC or UBC)

5. Baranowski T, Abdelsamad D, Baranowski J, O’Connor TM, Thompson D, Barnett A, Cerin E, Chen TA. Impact of an active video game on healthy children’s physical activity. Pediatrics. 2012;129(3):e636-642 (View)

6. Lipnowski S, LeBlanc CMA, Canadian Paediatric Society, Healthy Active Living and Sports Medicine Committee. Healthy active living: Physical activity guidelines for children and adolescents. Paediatr Child Health 2012;17(2):209-10 (View)

7.  http://www.physicalactivityline.com/

Note: We have been informed that use of online storage services does raise some concerns regarding protection of privacy (Freedom of Information and Protection of Privacy Act – FIPPA), especially due to the fact that data on these services is more than likely to be stored outside of Canada.  In addition to potential risk of data/security breaches from the internet at large, governments also have varying policies and powers regarding access to private data stores.  With this in mind, we would reiterate that it is critical to not store patient or other private information on cloud storage services.  In addition, to respect copyright, when sharing articles, users should only send the citations (eg. PMID, DOI or web citation) rather than the actual files.

What I did before

Like many physicians, for many years now, I’ve been using electronic-only copies of journal articles (pdf files) for my own continuing education, reference and teaching purposes.  When discussing the latest clinical trials with trainees, I’d often email them articles for discussion.  In order to always have these available, I would store them on a USB flash memory key, or upload them to my MobileMe iDisk account, then access and download them as needed.

While this works well, it did require me to always remember to update my flash drive when the newest guideline came out, or find a computer that could access my web account, then paste the file or link to an email.  This is was often not possible because of the very restrictive computer policies at hospitals.

This app changed my practice

Dropbox app article by Dr. Steve Wong for TCMP

Dropbox (www.dropbox.com) is a free web service that offers users a 2GB (or 2.5 GB with a referral link* – http://db.tt/HZEQPHT ) storage repository on the web (“cloud storage” is the emerging term for services like this).   There are paid plans ($99USD/year for 50GB), but I suspect for the majority of users, the free accounts offer plenty of space.  Once installed on your computer, a new folder called “Dropbox” is created.  Anything you put in this folder synchronizes to the web.

The biggest advantage to Dropbox is its ubiquity.  The service can synchronize the contents of your Dropbox to any and all of your computers (Mac, PC, Linux) as well as any of your mobile devices (iOS – iPhone, iPad, iPod, Android and Blackberry), and is accessible from any web browser.

The synchronization feature is automatic and ensures your content is always up to date at all of your access points.   Sync is important because it allows you to access the files when not connected to the internet.  On computers, the files will be current as of the last time it was connected to the internet.  On a mobile device like an iPad, you can set favorite files from the Dropbox app that will remain in the device’s local storage even when it is not connected to WiFi (note you need to flag the specific file(s) you want stored locally beforehand).

In addition, Dropbox just introduced a sharing feature that allows users to send download links to anyone, even if they don’t have a Dropbox account.  This allows users to share files that are too large to send via email, and since the sharing link can be sent from the web browser, restrictive IT policies won’t get in the way of sharing a file (these policies often restrict computers from saving any files from the internet or attach them to emails being sent out).

Dropbox also has an interesting versioning feature built in.  This saves all versions of a file that you’ve uploaded to the service, so, for example, if you’ve made edits to a Powerpoint or Word file and for some reason need to revert or look at the original version, you can log onto the website and look at the edit history.

There are several other cloud storage services (Sugarsync, box.net, Amazon Cloud Drive, Microsoft SkyDrive), and some offer more storage than Dropbox for free, or are less expensive for paid plans.  You can read a good comparison here: http://lifehacker.com/5786884/cloud-storage-faceoff-windows-live-skydrive-vs-dropbox-vs-amazon-cloud-drive

None of the other cloud services have as many supported apps as Dropbox.   Many apps on iOS and Android use Dropbox as a storage drive, so that edits done on your PC, cell phone or tablet are always reflected no matter where you access them.

What I do now

Here are examples of my own use of Dropbox:

• I keep a folder of “Teaching Files” with over 150 journal articles and guidelines that I can pull up during teaching rounds or send links for further reading.  I’ve often emailed the articles to the residents before we’ve even finished discussing the case.
• As I identify and download journal articles that I want to read, either on my computer at the office or home, or on my iPad, I save them to my Dropbox account as I go.  I have a folder called “Reading List” to store these in until they are read and moved into “Teaching Files,” for example.
• I use my iPhone to take pictures and video of interesting pathology (eg. clubbing of the fingers, asterixis in encephalopathy) and then show these to trainees during teaching rounds, using either the iPhone screen for 1-3 trainees, or the projected computer in the morning report room for larger groups. Edit: I have now heard this could bring up FIPA (Freedom of Information and Privacy Act) privacy concerns, even with patient permission to use the images, so I will no longer be using Dropbox to hold patient images (even non-facial images can contain identifiable cues like jewelry, moles, tattoos, etc).
• Most of my Powerpoint presentations and handouts are too large for email services (many email services max out at 5MB) so instead of attaching the file, I send an email with a “Sharing Link” generated by Dropbox.
• I store presentation files on Dropbox, but edit them on either my home computer or laptop.  That way, the latest version is always being worked on, and I don’t have to worry about making sure I copied it to the laptop in time for the conference.  If disaster strikes (eg. my laptop won’t boot, is stolen, or won’t connect to the projector), I can then download the talk onto my iPhone and present from there (using an iPhone to VGA cable), or use a computer at the conference site with internet access and get the latest file from the web.
• I keep copies of relevant Pharmacare special authority forms (prefilled with my data), scanned requisitions and patient handouts so that they can be accessed from my office in Vancouver or in Richmond.  This saves time and desk clutter since I don’t need to keep the pads of reqs physically at my desk.

You can get pdf versions of Pharmacare special authority forms at:

https://www.health.gov.bc.ca/exforms/pharmacare.html

I do caution against storing private data (patient records, financial information, etc) on cloud services unless you first encrypt the file with a strong password.  Any time you have data “in the cloud” there is a risk of exposing that information.  Last year, Dropbox did report a 4 hour lapse in their login security mechanism that they reported affected fewer than 100 users, but this does drive home the fact that we must always be mindful of securing patient and personal data.

The availability of backed-up, always accessible data paired with mobile devices having ubiquitous internet access will fundamentally change how we manage information and educational resources.

Get Dropbox for free (2GB storage) at: www.dropbox.com

Or, use this referral link for 2.5GB storage free: http://db.tt/HZEQPHT

* Disclosure: referral links earn both you and the referrer (me) an extra 500 MB.  I am already at or near my maximum referral bonus, and there are no financial or other rewards for referrals.

Tech Tips: Installation

1. Get Dropbox for free (2GB storage) at: www.dropbox.com. Or, use this referral link for 2.5GB storage free: http://db.tt/HZEQPHT. See my disclosure above.
2. While Dropbox is available for mobile devices, it’s best to set it up on your computer first.  Once you have the Dropbox folder set up, you can simply copy files that you want backed up and synced to the Dropbox folder.
3. Set up folders within Dropbox like “Forms”, “Reading List”, “Videos”, “Pictures”, “Patient Handouts”, “Journal Articles”, etc.
4. You simply organize files by moving them into relevant file folders on your computer, and the Dropbox program will reflect these changes on all devices automatically.  Unfortunately, the mobile apps don’t move files between folders.  This is how I move files from my “Reading List” folder to the “Teaching Files” folder once I’m done.
5. You can get pdf versions of Pharmacare special authority forms at: https://www.health.gov.bc.ca/exforms/pharmacare.html.
6. I prefer to save files as pdf documents. This way, formatting is preserved and is readable almost anywhere – the end user does not need to have the original program to see the file, just a pdf reader application (built in on Macs, Adobe Reader is freely downloadable for PCs at adobe.com).  I save patient handouts, Word documents, Keynote and Powerpoint documents, and webpages as pdfs.
   The easiest way to convert files to pdf format is to use your computer to “print” the file as a pdf.  That way, any content you can print out can be saved as a properly formatted pdf document.
   On a Mac, this functionality is built in.  Choose to “Print” any file, then click the “PDF” box in the lower left hand side of the print dialog box.  Then, choose your Dropbox folder to save to.
   On a PC, get any program which can print pages as pdf documents to do the same thing (I like CutePDF, a free PDF print program – http://www.cutepdf.com/Products/CutePDF/writer.asp), choosing the installed “CutePDF Printer” as your printing device, then saving the file to your Dropbox.
7. Don’t put private data without encryption on cloud storage services.

Other Resources:

www.Dropbox.com

Referral link for 2.5GB storage free: http://db.tt/HZEQPHT (see disclosure statement above)

Round up of cloud storage services: http://lifehacker.com/5786884/cloud-storage-faceoff-windows-live-skydrive-vs-dropbox-vs-amazon-cloud-drive

Dropbox security lapse:  http://blog.dropbox.com/?p=821

Adobe Reader (to read pdfs on the computer): http://get.adobe.com/reader/

CutePDF – print to a pdf file (free): http://www.cutepdf.com/Products/CutePDF/writer.asp

What I did before

As a GP with a special interest in Diabetes and a long-term firm believer in the benefits of regular exercise it’s fair to say I devote much time and effort to encouraging my patients to find time to be active, to eat a healthy diet (with a vegetarian emphasis), and to continue their efforts at weight loss.

Type 2 diabetes (T2D) is a lifestyle disease. Therefore it is reasonable that the first goal of management is to encourage lifestyle change to reduce or reverse the underlying metabolic derangements. Most emphasis has been placed on obesity and weight loss as they are the 2 key factors in the cause and prevention/management of Type 2 diabetes.

Weight loss is incredibly difficult for most people to achieve and maintain. I regularly see patients stressed out at their failed efforts to lose weight. Most overweight patients, despite all exhortations, have given up trying because it ends in failure, makes them depressed and adds to the negative image they may already have of themselves.

What changed my practice

In 2009 at the World Diabetes Congress in Montreal I was invited to debate the relative merits of exercise vs. diet in the management of diabetes. I opted to argue for “exercise”.

Preparing for this debate was enlightening. A fascinating paper by Ross and Janiszewsky raised the question “Is weight loss the wrong goal?” (3). I’m now inclined to believe that it is!

The obesity epidemic has spawned a multibillion dollar diet industry. Diets come and go, with little solid evidence of long term benefit. Conversely the benefits of exercise are powerfully evidence based. Compelling data indicate that regular physical activity may be at least as important as diet in terms of both prevention of diabetes and avoidance of complications – especially heart attacks and strokes, which account for up to 80% of deaths. (1, 6)  In diabetes, low fitness far exceeds the risks associated with modest obesity and is one of the strongest predictors of all-cause mortality, considered to be on a par with smoking. (4) Physical activity can be as powerful as glucose lowering medication with fewer side effects. (5) High quality studies show many of the benefits of increased physical activity are independent of weight loss and include not only multiple physical benefits (including a reduction in certain forms of cancer, dementia, osteoporosis) but also the very significant benefits on quality of life, mood and wellbeing, self-esteem, insight, and overall enhanced coping skills in managing and living with a chronic disease such as diabetes.

It is no exaggeration to say that regular exercise is the cheapest, safest and most effective means to long term health. Inactivity or “sedentariness” may be public health enemy #1!

What I do now

I direct more effort to encouraging physical activity as a critical tool in the management of T2D. I emphasize a healthy diet but stress that weight loss is not the primary goal.  (“Waist loss” is a more useful concept and indicates a drop in visceral obesity – a powerful indicator of CV risk (2) I use a measuring tape in preference to scales.)

I emphasize that diabetes is a complicated disease that requires complicated treatment and an informed and aggressive approach from both physician and patient alike. The patient is the primary stakeholder – his diabetes is his responsibility. Multiple drugs are essential, but so too is a firm commitment to a lifestyle that includes prioritizing at least 30 mins a day to brisk walking or an equivalent form of exercise.

The evidence is unequivocal. We should all put far more emphasis on encouraging patients to be more active. A commitment of 30 mins in 24 hours is not huge and even if (as is likely for many) there is no weight loss, the multiple other benefits must be stressed.

I encourage patients to make that 30 mins in their day a priority time – “see it as an investment in your arteries – more vital to you than an investment in your bank account”  A pedometer is an inexpensive and powerful motivator for many people. The goal is 10,000 steps a day. (7)

I give my patient a preprinted  prescription using the “FITT” concept : Frequency 5 days/week; Intensity moderate to vigorous ie can converse without being overly short of breath; Time 30 mins per day; Type Aerobic 5/7 Resistance 3/7 (aerobic exercise 5 days per week and resistance exercise 3 days  per week).

I tell my patients it is better to be fat and fit than lean and unfit. I frequently remind them of the benefits of regular activity other than weight loss, viz a reduction in cardiovascular risk, improved lung function, stronger muscles and bones, a reduced risk for various types of cancer and an overall increase in energy level. There is probably no system in the body that is not damaged by diabetes. Conversely there is probably no organ system in the body that does not benefit from regular exercise.

Until very recently the hard evidence for the benefits of exercise was vague and ill defined. That has all changed – the benefits of an active lifestyle cannot be overstated.

*For a unique and fascinating overview please check out reference (8)

References: (Note: Article requests might require a login ID with CPSBC or UBC)

1. Lee DC, Sui X, Church TS, et al. Changes in fitness and fatness on the development of cardiovascular disease risk factors. J Am Coll Cardiol 2012; 59:665-672. (View article with CPSBC or UBC)
2. Leiter LA, Fitchett DH, Gilbert RE, Gupta M, Mancini GBJ, McFarlane PA and Ross R, and the working group.  Identification and Management of Cardiometabolic Risk in Canada: A Position Paper by the Cardiometabolic Risk Working Group (Executive Summary) Cdn J Cardiol 27(2): 124-131, 2011. (View article with CPSBC or UBC)
3. Ross R, and Janiszewski PM. Is weight loss the optimal target for obesity-related cardiovascular disease risk reduction?  Cdn J Cardio 24:  25D-31D, 2008 (View article with CPSBC or UBC)
4. Church TS et al.  Exercise capacity and body composition as predictors of mortality among men with diabetes..Diabetes Care 2004;27(1);83-88 (View)
5. Knowles WC et al Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin  N Engl J Med. 2002; 346(6;) 393-403 (View)
6. CDA 2008 CPG for the Prevention and Management of Diabetes in Canada :Can J Diabetes 2008; 32(suppl1) S1-S201 (View)
7. Tudor-Locke, Catrine (June 2002). “Taking Steps toward Increased Physical Activity: Using Pedometers to Measure and Motivate” <http://www.fitness.gov/pcpfsdigestjune2002.pdf>. President’s Council on Physical Fitness and Sports Research Digest, Washington, DC
8. 23 1/2 hours – Dr. Mike Evans. website http://www.myfavouritemedicine.com/

Additional reading:

http://www.bcguidelines.ca/guideline_diabetes.html

http://www.health.gov.bc.ca/pharmacare/pdf/infosheet-on-diabetes-therapy.pdf

What I did before

When faced with most asthma exacerbations my practice was often to treat with oral steroids for 7 days along with a salbutamol inhaler and leave the discussion regarding the prescription of a steroid inhaler to their family physician that they were to follow-up with.  I never thought that the addition of an inhaled corticosteroid would add anything if they were taking it orally.

What changed my practice

I had a case of a young lady who I treated with salbutamol and prednisone and had follow-up at the end of her course of prednisone.  She made an appointment for the day after the prednisone was completed.  She presented to her family doctor in such respiratory distress that she had to be referred back (to me) and spent several hours in the Emergency Department and ultimately being admitted.  Although in the end, she did well, this led me to reconsider how I treated asthma exacerbations and based on an article by Dr Brian Rowe, I have now made it routine practice to prescribe both oral and inhaled steroids to my asthma patients on discharge.

In 1999, Rowe, from Edmonton, published a definitive study on the role of inhaled steroids in the acute asthma exacerbations.  It was a placebo controlled double-blind randomized trial involving 1006 consecutive patients age 16 – 60 years and after excluding those already on steroids, 188 were enrolled in the study.  All patients received oral prednisone 50 mg/day for 7 days and received either inhaled budesonide 1600 μg/d or placebo for 21 days.  After 21 days, 12 (12.8%)of 94 patients in the budesonide group experienced a relapsecompared with 23 (24.5%) of 94 in the placebo group, a 48% relapsereduction (P=.049).

What I do now

Given their effectiveness, safety, and ability to prevent relapses inhaled corticosteroids are now part of my discharge prescription for asthma exacerbations.  I further justify it because some patients may not be able to follow up with a family physician and because this approach reinforces the value of inhaled steroids to the patient.

Additional reading:

1. BC Guideline on Asthma: http://www.bcguidelines.ca/guideline_asthma.html#recommendation3 
2. FitzGerald JM. Asthma guidelines: Global to local. Ann Thorac Med [serial online] 2009 [cited 2012 Apr 30];4:161-2. Available from: http://www.thoracicmedicine.org/text.asp?2009/4/4/161/56006

Reference:

Rowe BH, Bota GW, Fabris L, et al. Inhaled budesonide in addition to oral corticosteroids to prevent asthma relapse following discharge from the emergency department: a randomized controlled trial. JAMA 1999; 281:2119–2126

http://jama.ama-assn.org/content/281/22/2119.full.pdf+html or with CPSBC

What I did before

As a family doctor in practice for 28 years providing maternity care, I thought I knew my patients well. I cared for them through young womanhood, pregnancies, and childbearing with numerous opportunities for therapeutic encounters. I spend a lot of time talking with and listening to my patients. Although I am well aware that usual care by family doctors fails to recognize 30-50% of depressed patients, I was sure this did not apply to my practice. When screening for depression at 28-32 weeks with the Edinburgh Depression Scale was incorporated into the BC Prenatal Record over a year ago, like most of my colleagues feeling short of time at the office, I never got around to administering it.

What changed my practice

I had recently completed a project with an interdisciplinary group creating the BC Maternity Care Pathway, which reviewed and summarized guidelines for routine prenatal care based on current evidence. Since I was one of the authors I decided I had better implement all of the recommendations into my practice. With an inward sigh I gave the EDS to every pregnant woman I saw between 28 and 32 weeks. The very first week I used it I was humbled to discover two cases of severe mood disorder.

The first was a 26 year old woman pregnant for the second time. She had had an exhausting and strenuous 3 years with her first child who had a “difficult” temperament. However, other than fatigue and the expected stress, I thought she was coping quite well.  I handed her the EDS and got back a score of 24 out of a possible 30, which on this scale is “severe”. My eyebrows raised and I asked, “Can you tell me more about feeling very low?”  She immediately burst into tears and poured out a story of insomnia, fear, anxiety, guilt, and despair going back to a childhood of extreme neglect and abuse.  I was shocked that I didn’t know any of this and realized she must have suffered silently during her first pregnancy. When asked if she would like help with this, she was relieved.

The next day a similar patient interaction with a 36 yr old nulliparous woman, resulted in an EDS with a very high score for anxiety. Again the unexpected revelation of distress in this high functioning woman surprised me.  I had inquired about mood throughout the pregnancy, without ever identifying that which was revealed to me via the EDS.

Mental illness is common in pregnancy and the postpartum period affecting as many as 25% of women, with depression and anxiety being the most common problems. Some investigators have reported obstetric complications associated with depression in pregnancy such as an increase in preterm labour, substance misuse, both high and low weight gain, and poorer performance on neonatal assessment tests. Infants of depressed mothers show delayed neurologic, cognitive, psychological, and motor development. When the mother’s mental illness is in remission the child’s behavioral and cognitive disorders improve.  In women with perinatal mental illness there is an associated increase in poor socioeconomic status (no educational qualifications, unmarried, unemployed) and increased intimate partner violence (IPV). Antenatal depression is associated with an increased incidence of postnatal depression and thus early identification can help women and their care-providers plan for extra support and surveillance . Women with a prior history of perinatal depression have a 30-50% chance of recurrence with a subsequent pregnancy. These are the women at greatest risk of suicide. It is therefore compelling to recognize and treat women with perinatal mental illness. Due to frequent contact with health care providers, pregnancy is an ideal time to provide support, treatment, and close monitoring.

The EDS is a highly sensitive screening tool administered in less than 10 minutes and can be distributed before the encounter.  It has been validated in pregnancy. The questions on the EDS make it suitable for screening in pregnancy, as there is less focus on somatic symptoms. The evidence that screening and providing treatment for perinatal mental illness improves outcomes remains equivocal. However ACOG, NICE (UK), U.S. Preventive Services Task Force and the Perinatal Services of BC in the Maternity Care Pathway all recommend formal screening for depression in pregnancy due to its serious morbidity and the potential for benefit to an individual woman and her family.

What I do now

Since that first week of using the EDS I now employ it on all my patients and continue to discover far more symptomatology than I did before. For some women the questionnaire is an education tool and they become aware of the extent of their distress and re-examine their lifestyle and supports. For others it offers an important opportunity to make the practitioner aware of problems and thus be able to assist in treatment, identify co-morbidities such as IPV, and hopefully prevent further progression.  I no longer trust that I “know” my patients and utilize formal screening for antenatal mental health. Next I am implementing the alcohol-screening tool TACE routinely!

Additional materials:

Edinburgh Postnatal Depression Scale 1 (EPDS) http://www.fresno.ucsf.edu/pediatrics/downloads/edinburghscale.pdf

BC Maternity Care Pathway  http://www.bcprenatalscreening.ca/sites/prenatal2/files/Guideline_19.pdf

BC Clinical Practice Guidelines (CPG’s) http://www.perinatalservicesbc.ca/Guidelines/default.htm

References: (Note: Article requests might require a login ID with the BC College of Physicians website or UBC)

1. Simon GE, VonKorff M. Recognition, management, and outcomes of depression in primary care. Arch Fam Med 1995; 4:99-105  (View article with CPSBC or UBC)
2. June C. Carroll, Anthony J. Reid, Anne Biringer. Effectiveness of the Antenatal Psychosocial Health Assessment (ALPHA) form in detecting psychosocial concerns: a randomized controlled trial. CMAJ • AUG. 2, 2005; 173 (3)
3. Evans J, Heron J, Francomb H, et al. Cohort study of depressed mood during pregnancy and after childbirth. BMJ 2001;323:257-60  (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC35345/pdf/257.pdf)
4. Gaynes BN, Gavin N, Meltzer-Brody S, et al. Perinatal depression: prevalence, screening accuracy, and screening outcomes. Evid Rep Technol Assess (Summ) 2005; Number 119:1-8  (http://www.ncbi.nlm.nih.gov/books/NBK37740/)
5. Gjerdingen DK, Yarn BP. Postpartum depression screening importance, methods, barriers and recommendations for practice.  J. Am Board Fam Med 2007; 20:280-8  (http://www.jabfm.org/content/20/3/280.full.pdf+html)
6. Weissman, MM, Pilowsky DJ, Wickramaratne, PJ, Talati A, Wisniewski SR, Fava M, et al.  Remissions in maternal depression and child psychopathology: a STAR*D-child report.  STAR*D-Child Team [published erratum appears in JAMA 2006:296:1234].  JAMA 2006:295:1389-98  (View article with CPSBC or UBC)
7. Wilson LM, Reid AJ, Beringer A, Carroll JC, Stewart DE.  Antenatal psychosocial risk factors associated with adverse postpartum family outcomes.  Canadian Medical Association Journal 1996; 154: 785-99  (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1487795/pdf/cmaj00090-0043.pdf)
8. Lewis G, Drife J, editors. Why mothers die 1997-1999: the fifth report of the Confidential Enquiries into Maternal Deaths in the United Kingdom. London: RCOG Press; 2001  (Book- available at Woodward library: WA900.FA1 W499 1998)
9. Murray D, Cox JL. Screening for Depression during pregnancy using the Edinburgh depression Scale. Journal of Reproductive and Infant Psychology 1990; 8:99-107  (IK Barber Learning Centre ASRS Storage  BF719 .J687)
10. Cochrane review 2008,  Antenatal psychosocial assessment for reducing perinatal mental health morbidity  http://www2.cochrane.org/reviews/en/ab005124.html (View article with CPSBC or UBC)
11. Committee Opinion No. 453: Screening for Depression During and After Pregnancy.  Obstetrics & Gynecology: February 2010 – Volume 115 – Issue 2, Part 1 – pg 394-395  (View article with CPSBC or UBC)
12. NICE Clinical guideline: Antenatal Care: Routine care for the healthy pregnant woman.  National collaboration /Center for Women’s and Children’s Health, Clinical Guideline; March 2008, chapter 7.6 Psychiatric screening.  P.118  (http://www.nice.org.uk/nicemedia/pdf/CG062NICEguideline.pdf scroll or search for ‘sec2:118′)

What I did before:

According to Osteoporosis Canada, as many as 2 million Canadians suffer from osteoporosis.  We can share with our patients that one in four women over the age of 50 has osteoporosis and at least one in eight men over 50 also osteoporosis.  Finally, less than 20% of patients with a fracture after the age of 50 are assessed and treated for osteoporosis!¹ The biggest challenges are motivating our patients to prevent a fracture given it is a silent disease and even convincing those with a prior fragility fracture to initiate and continue with treatment. Given our aging population, more and more family physicians are being asked for advice about diagnosis and treatment on osteoporosis.  With the time constraints of family practice, I often felt overwhelmed by identifying the right patient, pressured to give enough information, challenged to review the clinical trials and only having to rely on BMD results.

What changed my practice

These things changed my practice regarding osteoporosis management in primary care:

1. 2010 Osteoporosis Canada Guidelines and free CAROC electronic mobile device 10 year risk calculator app²
2. World Health Organization FRAX® website³, free online10 year risk calculator and paid app⁴
3. 2011 BC Guidelines and Protocol Advisory Committee Osteoporosis Guidelines available for free on the web and free BC Guidelines App on iTunes⁵

What I do now

Facing a patient and/or their families in the examination room, the common themes family physicians face are:

1. Motivating our patients by giving them an individual fracture risk assessment at the point of care
2. Determining which investigations are appropriate
3. Providing patients with education and resources on the disease
4. Effectively counseling them on lifestyle/non-pharmacologic and pharmacologic options to treat their disease and develop a long term plan for reassessment.

By being aware and utilizing both of the BC and National Osteoporosis practice guidelines and a combination of the free and/or paid apps available, I’m able to offer my patients complementary and mostly concordant advice about identification of risk factors, their individual 10 year fracture risk and options for treatment and investigations. In fact, using either online FRAX® calculator or Osteoporosis Canada CAROC hand held device application from the point of care helps me provide my patients with an idea of their approximate 10 year absolute fracture risk if they are naïve to therapy based on Canadian data. As a family physician, you may choose one, two or all of the tools and online resources depending on your practice style and patients. Access to the guidelines from the point of care allows me to tackle the various patients concerns and questions with reference material. Also, depending on your style, you can choose to squeeze all of this into one 15 minute appointment or negotiate with our patient to come back to review separate components in manageable sections or chunks.

I like the free Osteoporosis Canada mobile app (CAROC)  http://itunes.apple.com/ca/app/10-year-fracture-risk assessment/id434296900?mt=8 as it is quick and easy to use in real world practice.

Also, it is endorsed by the Canadian Radiology Association.  The calculator requires the clinician enter risk factors of age, sex, history of fracture, BMD results and information on glucocorticoid use. As you enter values into the calculator, the slider on the bottom moves left and right to show you and the patient their 10 year risk for having a fracture, which helps me inform my patients about the rationale to either recommend or postpone therapy. One further button toggle and this app gives me the ability to explain the guideline recommended therapeutic options including exercise and prevention of falls, Calcium and Vitamin D recommendations and presents an easy to use table for first line recommendations for pharmacologic therapy.  Finally, this IOs app gives me access to the full text guidelines, executive guideline summary, recommendations for lab investigations and factors modifying patients at moderate (10-20%) 10 year risk for fracture.

I like the free online World Health Organization FRAX® website calculator as it gives me the ability to give my treatment naïve patients their 10 year absolute risk probability of having a major osteoporotic or hip fracture. You can calculate the absolute risk with our without BMD measurement (although without a BMD value, the tool is unvalidated).

One must have access to the internet via a computer in the exam room, but you can print up the results for the patient to review. In addition, this model integrates other independent risk factors including past history of fracture, parental history of fracture, smoking, rheumatoid arthritis, and alcohol use as well as the other osteoporotic risk factors. A paid application is available, http://itunes.apple.com/ca/app/frax/id370146412?mt=8

I like the free online BC GPAC guidelines (GPAC = Guidelines and Protocols Advisory Committee) as it offers me the ability to review assessment of risk, risk stratification, lifestyle advice, therapy all in one place as well as give me access to printable patient education materials. The free mobile device osteoporosis app will be available in early April 2012.⁷

The bottom line is guidelines, websites and electronic apps are simply meant to support and to enhance, never replace the doctor patient relationship and communication.  The information at the point of care can help me to justify my recommendations and they add some credibility. These resources can help to share the responsibility for managing this chronic disease with our patients by giving them the information for improved informed decision making.

1)  http://www.osteoporosis.ca/multimedia/guidelines.html

2)  http://itunes.apple.com/ca/app/10-year-fracture-risk assessment/id434296900?mt=8

3)   http://www.shef.ac.uk/FRAX/

4)   http://itunes.apple.com/ca/app/frax/id370146412?mt=8

5)   http://www.bcguidelines.ca/guideline_osteoporosis.html

6)   http://itunes.apple.com/ca/app/bc-guidelines/id377956292?mt=8

7)   http://www.sigmamenopause.com/: The Canadian Menopause society, SIGMA, is an independent, multidisciplinary group of family physicians and specialists interested in menopausal and postmenopausal health. The Sigma website has a series of FAQ documents directed to patients to answer questions about different treatments including HRT, various anti-resportive agents and bioidentical hormones.

Special thanks to Dr. David Kendler and Dr. A Papaioannou for reviewing and providing their comments and suggestions.

What I did before

As patients with multiple co-morbidities age and their medical conditions become more debilitated, they face significant challenges in their day to day living.  Over my 25 years in full service family practice, I would try to manage their multiple medical conditions balancing the various clinical practice guideline recommendations against the individual patient needs and wishes.  Unfortunately, the discussion of advance care planning was time consuming and often only dealt specifically with the patient’s feelings about “code status”.  Often this only came once the patient had experienced a significant episode of decompensation (a sentinel event) that resulted in a trip to the ER or even hospitalization.  While I was aware of the “No Cardiopulmonary Resuscitation” form and the BC Palliative Care Benefits Program application, I was not aware of other tools to assist me with this discussion.  Like many physicians, I thought palliative care and end of life discussions were appropriate primarily for cancer patients.

What changed my practice?

In 2007, the GP Services Committee developed the Complex Care Planning fee (14033) to encourage Family Physicians to spend time with patients with multiple co-morbidities and develop a plan for their management.  At this planning visit, the FP discusses a patient’s wishes and desires for their future care, including end-of-life care and which life-prolonging medical interventions they might wish to have or refuse if they become incapable of deciding later.  An advance care plan (ACP) is developed with the patient that can then be reviewed on a regular basis and when their medical status changes.   Subsequent to this, the GPSC developed the Palliative Planning fee (14063) to compensate Family Physicians for developing a palliative care plan more specifically to address needs and wishes when a patient is felt to be in the last 6 months of life.  Both of these initiatives open the ability to provide follow-up medical management by telephone or 2 way e-mail.  FPs are also encouraged to conference with allied health professionals for the management of these patients and details of all the GPSC incentives can be found at http://gpscbc.ca/billing-guide-fees.  Specialists are not eligible to access the GPSC billing incentives, but the Specialist Services Committee is working on a similar incentive to encourage end of life planning.

More recently, the Practice Support Program has begun the “End-of-Life” PSP Module to encourage the earlier identification with the use of the “Surprise Question” (Would I be surprised if this patient were to die in the next 6 – 12 months?) and the development of a registry within the FP practice of patients who would benefit from a palliative approach to care.  It encourages the use of the “My voice” tool that was initially developed by the Fraser health Authority and is now the provincial Advance Care Planning tool.   This module also supports the integration of care (FP, Specialist, H&CC, Palliative Care and other supportive services) around the patient and family to encourage medically appropriate care and services at the end of life in the location preferred by most patients – their home.  More information can be found at http://gpscbc.ca/psp/learning.

What I do now

When caring for patients with multiple co-morbidities and/or cancer, I use the “Surprise Question” to develop a registry of patients who would benefit from a palliative approach to care so that I can identify and assess their symptoms and begin talking with them about their health status and goals of care at an earlier stage.  I use the “My Voice” tool and feel more comfortable asking them about their wishes in approaching this discussion.  Patients and their families have reported back that this reassures them that I am interested in their point of view and that they have confidence their wishes are going to be honoured.  Many are actually relieved that the topic has been raised,

Even if my answer to the surprise question would indicate the patient is not in the last 6 – 12 months of life, I am able to start the advance care planning conversation with patients when they are well.  At this stage, they are likely more able to make decisions about what they would agree to, or not, if in the future they are not able to make a decision for themselves.   I am also able to better access appropriate services to support them in their home through better coordination of care with my specialist colleagues as well as in the Home and Community Care program.  I feel I am able to provide better care for my patient and their family, as they progress in this final stage of their chronic disease management.

Resources

www.gpscbc.ca – All GPSC initiatives for billing and PSP modules can be found linked at this site.

http://www.bcmj.org/print/4158  – BCMA blog with links to other tools to support Advance Care Planning

https://www.bcma.org/news/advance-directives

www.health.gov.bc.ca/library/publications/year/2011/health-care-providers’-guide-to-consent-to-health-care.pdf  – BC Government Healthcare Providers guide to Consent

What I did before
Hemangiomas of infancy are soft tissue tumours that general practitioners and pediatricians commonly see in their practices. These growths occur in up to 2% of newborns.  They are benign vascular proliferations that typically undergo a growth phase (until approximately 6-12 months), followed by a plateau phase, and then enter a slow gradual involution phase. The general rule of thumb is that 50% are gone by 5 years, 70% by 7 years, and 90% by 9 years. It is important for the practitioner to discuss with the patient’s family that “gone” does not always mean that the area will later be completely normal.  After involution there can be variable amounts of residual hemangioma.  At times after involution, especially with large exophytic hemangiomas, there can be excess fibrofatty tissue that may require surgical revision.  Families can be reassured that hemangiomas are benign and often observation alone is all that is warranted.  In a patient with an uncomplicated hemangioma the physician can continue with normal routine health care. The family should be advised that if the lesion is not following the normal course or if there are concerns then earlier reassessment is warranted.  If there are complicating factors (e.g. associated bleeding or ulceration) and or special locations (e.g. Periocular, large facial, perineal) then active intervention and close follow up may be necessary…
The associated risk of each patient’s hemangioma needs to be weighed in order to decide if intervention is necessary.  If the clinician determines that the hemangioma places the patient in a life or function threatening situation * then treatment is necessary. A variety of treatments have been used for hemangiomas, but historically hemangiomas that put patients at serious risk have been treated with high dose oral corticosteroids (2- 5 mg/kg/day of prednisone), often for months.  This gold standard treatment has been effective for these serious hemangiomas, but it also placed our patients at risk of serious steroid side effects, such as suppression of growth, the immune system and the adrenal axis.
* Examples of life or function threatening hemangiomas include:  Periocular – visual complication; Beard distribution – airway involvement;  Perineal/perianal –ulceration/infection;  Sacral/large perineal – urogenital abnormalities/ imperforate anus;  Midline lumbrosacral – spinal dysraphism; Large segmental  hemangiomas-  may be associated congenital abnormalities in the segment; Large plaque type facial hemangiomas- PHACES syndrome = Posterior fossa abnormalities, Hemangioma, Arterial abnormalities, Cardiac, Eye abnormalities,  Sternal  cleft;  Multiple hemangiomas- Systemic hemangiomatosis, i.e. internal hemangiomas primarily liver.

What changed my practice
In 2008, oral Propanolol, a non-selective Beta blocker, was serendipitously noted to shrink hemangiomas present in cardiac patients 1.  This experience has been repeated by other groups and many pediatric dermatologists now use Propanolol instead of oral corticosteroids as first line therapy for serious hemangiomas. The use of Propanolol for hemangiomas is not without risks and its use has been reported to be associated with hypotension, bradycardia, bronchospasm, hypoglycemia and hypothermia 2, 3.  Different Pediatric centres have created a variety of treatment protocols that primarily differ in their monitoring, and rates of dosage increase and tapering.  In general, the dose usually starts at approximately 0.5 mg/kg/day and is slowly titrated up to 2 mg/kg/day.   In the future with ongoing research and clinical experience we will gain more knowledge on the rates of side effects, preferred dose and duration of treatment.  At that point firm recommendations regarding monitoring requirements and the setting in which the treatment can be best provided.  However, at this time, due to the above listed issues the use of oral propanol for hemangiomas should only be undertaken by those familiar with the treatment in association with close observation of the patient for potential side effects.
Additionally, there are some reports on the use of topical Timolol o.5% gel; a non-selective topical beta blocker commonly used for glaucoma, for the treatment of less worrisome hemangiomas 4, 5. The reports to date have demonstrated safety and efficacy.

What I do now
At present, for hemangiomas patients who I feel need systemic therapy I personally use oral Propanolol instead of systemic steroids, as I believe that the benefit risk analysis presently favours Propanolol.  If I think that a patient could potentially have a problem in the near future, I will often start a trial of topical Timolol with close observation for any progression of the lesion. A good example of this scenario would be a small periocular hemangioma that has no evidence of ocular effects based on pediatric ophthalmologic exam.  This early topical therapy may offset the need for systemic therapy in the future.
Timolol 0.5% has been used in the literature, but this concentration was chosen due to the fact that it is the commercially available concentration. While a small body of literature supports the use of Timolol 0.5% it is not clear whether this is the optimal concentration.  I initially used 0.5% but due to a partial response I subsequently increased the dose to Timolol 2% compounded into a gel.  The patients I have treated with Timolol 2% have demonstrated clinical benefit without parental reports of clinical side effects.  However, there is no present data on comparison of the efficacy of different Timolol concentrations.  Due to the issues of potential increase of cutaneous medication absorption in infants and the lack of data on the level of absorption through hemangiomas, when I first started using 2% Timolol I initially performed Timolol levels on my patients Reassuringly I was not able to demonstrate any measurable serum drug levels (to be published in future). In the future, as we gain more comfort with the safety and efficacy of topical Timolol we may be able to offer the option of treatment to patients/families that are experiencing significant psychosocial stress due to hemangiomas that are not threatening function. It may also become a useful agent for hemangiomas that are potentially at risk of future sequelae.  Theoretically if used early enough the growth of the at risk lesion may be controlled, thus potentially offsetting the need for systemic therapy.  Topical and oral Beta blockers are exciting new treatment options that have caused a paradigm shift in the treatment of hemangiomas away from steroid.

References (Note: Article requests require a login ID with CPSBC or UBC)
1)      Leaute-Labreze C  et al: Propanolol for severe hemangiomas of infancy.   N Engl J Med  2008; 358(24):2649-2651. (full text)
2)      Starkey E. Propanolol for infantile hemangiomas: A review.  Arch  Dis Child. 2011 Sep:96(9):890-3. (full text)
3)      Siegfried EC et al:More on propanolol for hemangiomas of infancy.   N Engl J Med  2008; 359(26):2846-2847. (full text)
4)      Pope E et al. Topical Timolol gel for infantile hemangiomas: a pilot study. Arch of Dermatol. 2010 May; 146(5):564-5. (full text)
5)      Ni N, Topical Timolol for periocular hemangiomas: a report of further study. Arch Ophthalmol 2011 Mar: 129(3):377-9. (View article with CPSBC or UBC)
6)      Ni N. Current concepts in the management of periocular hemangioma. Curr Opin Ophthalmol 2011 Sep; 22(5):419-25. (View article with CPSBC or UBC)
7)      Spiteri Cornish K. The use of Propanolol in the management of periocular haemangioma- a systematic review, Eye (Lond). 2011 ju 8:1-7. (View article with CPSBC or UBC)
8)      Zaher, H. Oral Propanolol: an effective, safe treatment for infantile hemangiomas. Eur J Dermatol 2011 Jul-Aug; 21(4):558-63. (View article with CPSBC)

What I did before

When I started treating breast cancer, systemic therapy recommendations were usually based only on the menopausal status of the woman and whether there was cancer in the axillary nodes.  Although estrogen status was being measured the importance of this marker was not appreciated.

What changed my practice

In the last decade there has been an explosion of information about the genetics and molecular makeup of breast cancers with a heightened understanding that breast cancer is not one disease. A landmark publication in 2000 described four types of breast cancer. ¹ In a recent as yet unpublished study using newer sequencing technology, researchers at the BC Cancer Agency and collaborators from the UK have suggested 9 distinctive types of the disease. ²  The recognition of these subtypes of breast cancer is changing how we approach and treat the disease.

The risk of recurrence is a major concern when an early breast cancer is diagnosed as even with excellent surgery there is a risk of both local and systemic recurrence.  Architectural factors such as the size of the tumour and nodal involvement have classically been used to determine risk. Biological features such as estrogen receptor status, HER2 expression and grade, often measured by Ki67, are now being included in our risk assessment.

The responsiveness of the tumour has also become an important determinant in how we treat the disease.  Responsiveness describes how the tumour will be affected by specific treatments.   For example, estrogen receptor status determines whether a breast cancer will respond to endocrine therapy; the gene HER2 is associated with response to anti HER2 therapy such as trastuzumab (Herceptin); and high KI67 tumours may be more responsive to chemotherapy than those with a lower grade or KI67.  Thus two similar sized tumours may get different treatment recommendations based on their biology.

What I do now

For patients with low grade estrogen receptor positive tumours I am recommending much less chemotherapy even if there is nodal involvement and/or the woman is premenopausal.  In these tumours, endocrine therapy may be the most effective treatment and chemotherapy may minimally impact survival.  Having said that, some patients still benefit from including chemotherapy in addition to hormone therapy.  For patients with HER2 overexpressing tumours I often recommend chemotherapy and trastuzumab even if the tumour is small with no involved nodes.  Understanding the biology of breast cancers is providing more personalized recommendations and this is translating into better outcomes.

As we further define subtypes, more targeted treatments will be developed but at this time for many cancers we continue to give broad cytotoxic therapy.  As well, new agents are being developed and may be further decrease recurrences. We are also now frequently rebiopsying recurrent cancers to further understand the markers of response and resistance and to tailor treatment. We also need to study the “host” patient, as the pharmacogenomics of the individual may affect how the drug is metabolized and also may contribute to the effectiveness and the toxicity of the therapy.

How does this affect family physicians?  Treatment recommendations may be more complicated so counseling patients prior to their oncological consultation may be more confusing.  It may be more difficult to know whether chemotherapy will be recommended or not especially if we begin to do more complex assessments of tumours in specialized laboratories. Numerous studies are reported in the lay and academic press and are never substantiated.  Understanding what is of relevance to the care and management of our patients and which data is transient is difficult.  We need to ensure that the government prioritizes an upgrade of our electronic BC Cancer Agency website and electronic record to make it accessible to primary health care providers with the appropriate, evidence based results.

Biological information is often available as soon as the core biopsy diagnoses an invasive cancer.  Early referral to centres with multidisciplinary teams may avoid long delays and confusing information for both the patient and the primary care providers.  Electronic integrated systems may also aid the transfer of information. Frequent updates at family practice meetings and in journals can also provide current treatment and care models to a wider audience.  With this knowledge, family practices can provide a broad idea of the concept of adjuvant therapy for the treatment of early breast cancer and introduce the idea of chemotherapy, hormones and radiation without specifying the details.  Family doctors should be aware of the new patient package, including a patient book that is available through the Alliance for Breast Cancer Information at the BC Cancer Agency. ³ Reassuring patients about the improvements in survival as over 90% of early breast cancer cases in BC now live over 5 years will also help provide helpful information to decrease a woman’s anxiety. 4

References (Note: Article requests require a login ID with CPSBC or UBC)

1. Perou CM, Sorlie T, Eisen MB, et al.  Molecular portraits of human breast tumours.  Nature 2000; 406 (6797): 747-52 (View article with CPSBC or UBC)
2. Personal communication with Dr Samuel Aparicio
3. Alliance for Breast Cancer Information BC, 604 707 5818, and Intelligent Patient Guide – Olivotto, Gelmon, McCready, 5^th edition, 2011 (book)
4. Coleman MP, Forman D, Bryant H et all.  Cancer survival in Australia, Canada, Denmark, Norway, Sweden and the UK, 1995-2007 (the international cancer benchmarking partnership): an analysis of population –based cancer registry data.  Lancet 2011; 377(9760): 127-138. (View article with CPSBC or UBC)

Cancer Care Outreach Program on Education (CCOPE)

Over the past 4 months, UBC CPD in partnership with BCCA and FPON has been delivering case-based workshops on breast cancer care to various communities in BC, the last workshop is scheduled for Dawson Creek on March 28^th.  Workshop contents covers screening guidelines, diagnostic procedures, main treatment options and their potential side effects, and follow-up of breast cancer patients.

Read more about the Cancer Care Outreach Program on Education (CCOPE) .

Read more about CCOPE – Breast Cancer Community Workshops.